Acute treatment with docosahexaenoic acid complexed to albumin reduces injury after a permanent focal cerebral ischemia in rats.

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Tiffany N Eady

Full Text Available Docosahexaenoic acid complexed to albumin (DHA-Alb is highly neuroprotective after temporary middle cerebral artery occlusion (MCAo, but whether a similar effect occurs in permanent MCAo is unknown. Male Sprague-Dawley rats (270-330 g underwent permanent MCAo. Neurological function was evaluated on days 1, 2 and 3 after MCAo. We studied six groups: DHA (5 mg/kg, Alb (0.63 or 1.25 g/kg, DHA-Alb (5 mg/kg+0.63 g/kg or 5 mg/kg+1.25 g/kg or saline. Treatment was administered i.v. at 3 h after onset of stroke (n = 7-10 per group. Ex vivo imaging of brains and histopathology were conducted on day 3. Saline- and Alb-treated rats developed severe neurological deficits but were not significantly different from one another. In contrast, rats treated with low and moderate doses of DHA-Alb showed improved neurological score compared to corresponding Alb groups on days 2 and 3. Total, cortical and subcortical lesion volumes computed from T2 weighted images were reduced following a moderate dose of DHA-Alb (1.25 g/kg by 25%, 22%, 34%, respectively, compared to the Alb group. The total corrected, cortical and subcortical infarct volumes were reduced by low (by 36-40% and moderate doses (by 34-42% of DHA-Alb treatment compared to the Alb groups. In conclusion, DHA-Alb therapy is highly neuroprotective in permanent MCAo in rats. This treatment can provide the basis for future therapeutics for patients suffering from ischemic stroke.

Novel pharmacokinetic studies of the Chinese formula Huang-Lian-Jie-Du-Tang in MCAO rats.

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Zhu, Huaxu; Qian, Zhilei; He, Feng; Liu, Mengzhu; Pan, Linmei; Zhang, Qichun; Tang, Yuping

2013-07-15

Our previous studies showed that after oral administration of an Huang-Lian-Jie-Du-Tang (HLJDT) decoction, there is a higher concentration of the pure components, berberine, baicalin and gardenoside in the plasma of Middle cerebral artery occlusion (MCAO) rats than in sham-operated rats, The aim of the present study was to determine whether these components could be reliably measured in MCAO rat tissues. First, the plasma concentration-time profiles of berberine, palmatine, baicalin, baicalein and gardenoside were characterised in MCAO rats after oral administration of the aqueous extract of HLJDT. Subsequently, liver, lung and kidney tissues were obtained from sudden death MCAO rats in the absorption phase (0.25 h), the distribution phase (1.0 h) and the elimination phase (8.0 h) after administration of the HLJDT aqueous extract. An HPLC method was developed and validated for the determination of the distribution characteristics of berberine, palmatine, baicalin, baicalein and gardenoside simultaneously from the above-mentioned rat tissues. The results indicated that berberine, palmatine, baicalin and baicalein distributed rapidly and accumulated at high levels in the lung, while gardenoside distributed widely in the lung and the kidney. To the best of our knowledge, this is the first report to describe the distribution of the active ingredients derived from HLJDT in MCAO rat tissues. The tissue distribution results provide a biopharmaceutical basis for the design of the clinic application of HLJDT in cerebrovascular disease. Copyright © 2012 Elsevier GmbH. All rights reserved.

The neuroprotective properties of the superoxide dismutase mimetic tempol correlate with its ability to reduce pathological glutamate release in a rodent model of stroke

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Dohare, Preeti; Hyzinski-García, María C.; Vipani, Aarshi; Bowens, Nicole H.; Nalwalk, Julia W.; Feustel, Paul J.; Keller, Richard W.; Jourd’heuil, David; Mongin, Alexander A.

2014-01-01

The contribution of oxidative stress to ischemic brain damage is well established. Nevertheless, for unknown reasons, several clinically tested antioxidant therapies failed to show benefits in human stroke. Based on our previous in vitro work, we hypothesized that the neuroprotective potency of antioxidants is related to their ability to limit release of the excitotoxic amino acids, glutamate and aspartate. We explored the effects of two antioxidants, tempol and edaravone, on amino acid release in the brain cortex, in a rat model of transient occlusion of the middle cerebral artery (MCAo). Amino acid levels were quantified using a microdialysis approach, with the probe positioned in the ischemic penumbra as verified by a laser Doppler technique. Two-hour MCAo triggered a dramatic increase in the levels of glutamate, aspartate, taurine and alanine. Microdialysate delivery of 10 mM tempol reduced the amino acid release by 60–80%, while matching levels of edaravone had no effect. In line with these latter data, an intracerebroventri-cular injection of tempol but not edaravone (500 nmols each, 15 minutes prior to MCAo) reduced infarction volumes by ~50% and improved neurobehavioral outcomes. In vitro assays showed that tempol was superior in removing superoxide anion, whereas edaravone was more potent in scavenging hydrogen peroxide, hydroxyl radical, and peroxynitrite. Overall, our data suggests that the neuroprotective properties of tempol are likely related to its ability to reduce tissue levels of the superoxide anion and pathological glutamate release, and, in such a way, limit progression of brain infarction within ischemic penumbra. These new findings may be instrumental in developing new antioxidant therapies for treatment of stroke. PMID:25224033

Dietary Virgin Olive Oil Reduces Blood Brain Barrier Permeability, Brain Edema, and Brain Injury in Rats Subjected to Ischemia-Reperfusion

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Fatemeh Mohagheghi

2010-01-01

Full Text Available Recent studies suggest that dietary virgin olive oil (VOO reduces hypoxia-reoxygenation injury in rat brain slices. We sought to extend these observations in an in vivo study of rat cerebral ischemia-reperfusion injury. Four groups, each consisting of 18 Wistar rats, were studied. One group (control received saline, while three treatment groups received oral VOO (0.25, 0.5, and 0.75 mL/kg/day, respectively. After 30 days, blood lipid profiles were determined, before a 60-min period of middle cerebral artery occlusion (MCAO. After 24-h reperfusion, neurological deficit scores, infarct volume, brain edema, and blood brain barrier permeability were each assessed in subgroups of six animals drawn from each main group. VOO reduced the LDL/HDL ratio in doses of 0.25, 0.5, and 0.75 mL/kg/day in comparison to the control group (p < 0.05, and offered cerebroprotection from ischemia-reperfusion. For controls vs. doses of 0.25 vs. 0.5 vs. 0.75 mL/kg/day, attenuated corrected infarct volumes were 207.82 ± 34.29 vs. 206.41 ± 26.23 vs. 124.21 ± 14.73 vs. 108.46 ± 31.63 mm3; brain water content of the infarcted hemisphere was 82 ±± 0.25 vs. 81.5 ± 0.56 vs. 80.5 ± 0.22 vs. 80.5 ± 0.34%; and blood brain barrier permeability of the infarcted hemisphere was 11.31 ± 2.67 vs. 9.21 ± 2.28 vs. 5.83 ± 1.6 vs. 4.43 ± 0.93 µg/g tissue (p < 0.05 for measures in doses 0.5 and 0.75 mL/kg/day vs. controls. Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, and improves neurologic deficit scores after transient MCAO in rats.

Inhibition of Cathepsins B Induces Neuroprotection Against Secondary Degeneration in Ipsilateral Substantia Nigra After Focal Cortical Infarction in Adult Male Rats

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Xialin Zuo

2018-05-01

Full Text Available Stroke is the leading cause of adult disability in the world. In general, recovery from stroke is incomplete. Accumulating evidences have shown that focal cerebral infarction leads to dynamic trans-neuronal degeneration in non-ischemic remote brain regions, with the disruption of connections to synapsed neurons sustaining ischemic insults. Previously, we had reported that the ipsilateral striatum, thalamus degenerated in succession after permanent distal branch of middle cerebral artery occlusion (dMCAO in Sprague-Dawley (SD rats and cathepsin (Cath B was activated before these relay degeneration. Here, we investigate the role of CathB in the secondary degeneration of ipsilateral substantia nigra (SN after focal cortical infarction. We further examined whether the inhibition of CathB with L-3-trans-(Propyl-carbamoyloxirane-2-carbonyl-L-isoleucyl-L-proline methyl ester (CA-074Me would attenuate secondary degeneration through enhancing the cortico-striatum-nigral connections and contribute to the neuroprotective effects. Our results demonstrated that secondary degeneration in the ipsilateral SN occurred and CathB was upregulated in the ipsilateral SN after focal cortical infarction. The inhibition of CathB with CA-074Me reduced the neuronal loss and gliosis in the ipsilateral SN. Using biotinylated dextran amine (BDA or pseudorabies virus (PRV 152 as anterograde or retrograde tracer to trace striatum-nigral and cortico-nigral projections pathway, CA-074Me can effectively enhance the cortico-striatum-nigral connections and exert neuroprotection against secondary degeneration in the ipsilateral SN after cortical ischemia. Our study suggests that the lysosomal protease CathB mediates the secondary damage in the ipsilateral SN after dMCAO, thus it can be a promising neuroprotective target for the rehabilitation of stroke patients.

Effects of gemfibrozil on outcome after permanent middle cerebral artery occlusion in mice.

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Guo, Qingmin; Wang, Guangming; Liu, Xiaowei; Namura, Shobu

2009-07-07

Fibrates are lipid lowering drugs and found as ligands for peroxisome proliferator-activated receptors (PPARs). A clinical study has shown that one type of fibrate gemfibrozil reduces stroke incidence in men. However, it remains unknown whether gemfibrozil improves outcome after stroke. We hypothesized that prophylactic administration of gemfibrozil improves outcome after ischemic stroke. In this study, we measured the impact of gemfibrozil in two permanent middle cerebral artery occlusion (MCAO) models in young adult male mice on normal diet. First, we tested gemfibrozil in a filamentous MCAO model. Pretreatment with gemfibrozil (30 mg/kg) for 7 days moderately but significantly reduced infarct size at 24 h after MCAO. A higher dose (120 mg/kg) did not attenuate infarct size. Rather, it tended to increase brain swelling. Second, we tested in a distal MCAO model. Gemfibrozil (30 mg/kg) for 7 days before and after stroke significantly attenuated cortical lesion size at 7 days after MCAO. Cortical blood flow measured by laser speckle imaging was improved by gemfibrozil in the ischemic hemisphere. In non-stroke animals gemfibrozil also altered gene expression levels of PPARs in both the aorta and brain in organ specific manners; however, endothelial nitric oxide synthase (eNOS) was not significantly affected. These findings suggested the possibility that the observed infarct reductions and cortical blood flow improvements in ischemic brains were not through eNOS-mediated mechanisms. Further investigations may be meritorious to examine whether prophylactic usage of gemfibrozil against stroke is beneficial.

Delayed treatment with ADAMTS13 ameliorates cerebral ischemic injury without hemorrhagic complication.

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Nakano, Takafumi; Irie, Keiichi; Hayakawa, Kazuhide; Sano, Kazunori; Nakamura, Yoshihiko; Tanaka, Masayoshi; Yamashita, Yuta; Satho, Tomomitsu; Fujioka, Masayuki; Muroi, Carl; Matsuo, Koichi; Ishikura, Hiroyasu; Futagami, Kojiro; Mishima, Kenichi

2015-10-22

Tissue plasminogen activator (tPA) is the only approved therapy for acute ischemic stroke. However, delayed tPA treatment increases the risk of cerebral hemorrhage and can result in exacerbation of nerve injury. ADAMTS13, a von Willebrand factor (VWF) cleaving protease, has a protective effect against ischemic brain injury and may reduce bleeding risk by cleaving VWF. We examined whether ADAMTS13 has a longer therapeutic time window in ischemic stroke than tPA in mice subjected to middle cerebral artery occlusion (MCAO). ADAMTS13 (0.1mg/kg) or tPA (10mg/kg) was administered i.v., immediately after reperfusion of after 2-h or 4-h MCAO for comparison of the therapeutic time windows in ischemic stroke. Infarct volume, hemorrhagic volume, plasma high-mobility group box1 (HMGB1) levels and cerebral blood flow were measured 24h after MCAO. Both ADAMTS13 and tPA improved the infarct volume without hemorrhagic complications in 2-h MCAO mice. On the other hand, ADAMTS13 reduced the infarct volume and plasma HMGB1 levels, and improved cerebral blood flow without hemorrhagic complications in 4-h MCAO mice, but tPA was not effective and these animals showed massive intracerebral hemorrhage. These results indicated that ADAMTS13 has a longer therapeutic time window in ischemic stroke than tPA, and ADAMTS13 may be useful as a new therapeutic agent for ischemic stroke. Copyright © 2015 Elsevier B.V. All rights reserved.

Breviscapine confers a neuroprotective efficacy against transient focal cerebral ischemia by attenuating neuronal and astrocytic autophagy in the penumbra.

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Pengyue, Zhang; Tao, Guo; Hongyun, He; Liqiang, Yang; Yihao, Deng

2017-06-01

Breviscapine is a flavonoid derived from a traditional Chinese herb Erigerin breviscapus (Vant.) Hand-Mazz, and has been extensively used in clinical treatment for cerebral stroke in China, but the underlying pharmacological mechanisms are still unclear. In present study, we investigated whether breviscapine could confer a neuroprotection against cerebral ischemia injury by targeting autophagy mechanisms. A cerebral stroke model in Sprague-Dawley rats was prepared by middle cerebral artery occlusion (MCAO), rats were then randomly divided into 5 groups: MCAO+Bre group, rats were treated with breviscapine; MCAO+Tat-Beclin-1 group, animals were administrated with specific autophagy inducer Tat-Beclin-1; MCAO+Bre+Tat-Beclin-1 group, rats were treated with both breviscapine and Tat-Beclin-1, MCAO+saline group, rats received the same volume of physiological saline, and Sham surgery group. The autophagy levels in infarct penumbra were evaluated by western blotting, real-time PCR and immunofluorescence 7days after the insult. Meanwhile, infarct volume, brain water content and neurological deficit score were assessed. The results illustrated that the infarct volume, brain water content and neurofunctional deficiency were significantly reduced by 7days of breviscapine treatment in MCAO+Bre group, compared with those in MCAO+saline group. Meanwhile, the western blotting, quantitative PCR and immunofluorescence showed that the autophagy in both neurons and astrocytes at the penumbra were markedly attenuated by breviscapine admininstration. Moreover, these pharmacological effects of breviscapine could be counteracted by autophagy inducer Tat-Beclin-1. Our study suggests that breviscapine can provide a neuroprotection against transient focal cerebral ischemia, and this biological function is associated with attenuating autophagy in both neurons and astrocytes. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Riociguat reduces infarct size and post-infarct heart failure in mouse hearts: insights from MRI/PET imaging.

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Carmen Methner

Full Text Available Stimulation of the nitric oxide (NO--soluble guanylate (sGC--protein kinase G (PKG pathway confers protection against acute ischaemia/reperfusion injury, but more chronic effects in reducing post-myocardial infarction (MI heart failure are less defined. The aim of this study was to not only determine whether the sGC stimulator riociguat reduces infarct size but also whether it protects against the development of post-MI heart failure.Mice were subjected to 30 min ischaemia via ligation of the left main coronary artery to induce MI and either placebo or riociguat (1.2 µmol/l were given as a bolus 5 min before and 5 min after onset of reperfusion. After 24 hours, both, late gadolinium-enhanced magnetic resonance imaging (LGE-MRI and (18F-FDG-positron emission tomography (PET were performed to determine infarct size. In the riociguat-treated mice, the resulting infarct size was smaller (8.5 ± 2.5% of total LV mass vs. 21.8% ± 1.7%. in controls, p = 0.005 and LV systolic function analysed by MRI was better preserved (60.1% ± 3.4% of preischaemic vs. 44.2% ± 3.1% in controls, p = 0.005. After 28 days, LV systolic function by echocardiography treated group was still better preserved (63.5% ± 3.2% vs. 48.2% ± 2.2% in control, p = 0.004.Taken together, mice treated acutely at the onset of reperfusion with the sGC stimulator riociguat have smaller infarct size and better long-term preservation of LV systolic function. These findings suggest that sGC stimulation during reperfusion therapy may be a powerful therapeutic treatment strategy for preventing post-MI heart failure.

Role of the NMDA receptor and iron on free radical production and brain damage following transient middle cerebral artery occlusion.

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Im, Doo Soon; Jeon, Jeong Wook; Lee, Jin Soo; Won, Seok Joon; Cho, Sung Ig; Lee, Yong Beom; Gwag, Byoung Joo

2012-05-21

Excess activation of ionotropic glutamate receptors and iron is believed to contribute to free radical production and neuronal death following hypoxic ischemia. We examined the possibility that both NMDA receptor activation and iron overload determine spatial and temporal patterns of free radical production after transient middle cerebral artery occlusion (tMCAO) in male Sprague-Dawley rats. Mitochondrial free radical (MFR) levels were maximally increased in neurons in the core at 1 h and 24 h after tMCAO. Early MFR production was blocked by administration of MK-801, an NMDA receptor antagonist, but not deferoxamine, an iron chelator. Neither MK-801 nor deferoxamine attenuated late MFR production in the core. Increased MFRs were observed in penumbral neurons within 6 h and gradually increased over 24 h after tMCAO. Slowly-evolving MFRs in the core and penumbra were accompanied by iron overload. Deferoxamine blocked iron overload but reduced MFR production only in the penumbra. Combined MK-801/deferoxamine reduced late MFR production in both core and penumbra in an additive manner. Combination therapy significantly ameliorated infarction compared with monotherapy. These findings suggest that the NMDA receptor activation and iron overload mediate late MFR production and infarction after tMCAO. Copyright © 2012 Elsevier B.V. All rights reserved.

Electro-acupuncture exerts beneficial effects against cerebral ischemia and promotes the proliferation of neural progenitor cells in the cortical peri-infarct area through the Wnt/β-catenin signaling pathway

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CHEN, BIN; TAO, JING; LIN, YUKUN; LIN, RUHUI; LIU, WEILIN; CHEN, LIDIAN

2015-01-01

Electro-acupuncture (EA) is a novel therapy based on combining traditional acupuncture with modern electrotherapy, and it is currently being investigated as a treatment for ischemic stroke. In the present study, we aimed to investigate the mechanisms through which EA regulates the proliferation of neural progenitor cells (NPCs) in the cortical peri-infarct area after stroke. The neuroprotective effects of EA on ischemic rats were evaluated by determining the neurological deficit scores and cerebral infarct volumes. The proliferation of the NPCs and the activation of the Wnt/β-catenin signaling pathway in the cortical peri-infarct area were examined. Our results revealed that EA significantly alleviated neurological deficits, reduced the infarct volume and enhanced NPC proliferation [nestin/glial fibrillary acidic protein (GFAP)-double positive] in the cortex of rats subjected to middle cerebral artery occlusion (MCAO). Moreover, the Wnt1 and β-catenin mRNA and protein levels were increased, while glycogen synthase kinase-3 (GSK3) transcription was suppressed by EA. These results suggest that the upregulatory effects of EA on the Wnt/β-catenin signaling pathway may promote NPC proliferation in the cortical peri-infarct area after stroke, consequently providing a therapeutic effect against cerebral ischemia. PMID:26329606

Effects of the combined treatment of bone marrow stromal cells with mild exercise and thyroid hormone on brain damage and apoptosis in a mouse focal cerebral ischemia model.

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Akhoundzadeh, Kobar; Vakili, Abedin; Sameni, Hamid Reza; Vafaei, Abbas Ali; Rashidy-Pour, Ali; Safari, Manouchehr; Mohammadkhani, Razieh

2017-08-01

This study examined whether post-stroke bone marrow stromal cells (BMSCs) therapy combined with exercise (EX) and/or thyroid hormone (TH) could reduce brain damage in an experimental ischemic stroke in mice. Focal cerebral ischemia was induced under Laser Doppler Flowmetry (LDF) guide by 45 min of middle cerebral artery occlusion (MCAO), followed by 7 days of reperfusion in albino mice. BMSCs were injected into the right cerebral ventricle 24 h after MCAO, followed by daily injection of T3 (20 μg/100 g weight S.C) and 6 days of running on a treadmill. Infarct size, neurobehavioral test, TUNEL and BrdU positive cells were evaluated at 7 days after MCAO. Treatment with BMSCs and mild EX alone significantly reduced the infarct volume by 23% and 44%, respectively (both, p cells (a marker of apoptosis) was significantly reduced in the EX, BMSCs, BMSCs + EX, BMSCs + TH, and BMSCs + EX + TH groups (all, p cells in the subventricular zone (SVZ) (p cells and the attenuation of apoptosis in ischemia stroke in young mice.

Misoprostol, an anti-ulcer agent and PGE2 receptor agonist, protects against cerebral ischemia.

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Li, Jun; Liang, Xibin; Wang, Qian; Breyer, Richard M; McCullough, Louise; Andreasson, Katrin

2008-06-20

Induction of COX-2 activity in cerebral ischemia results in increased neuronal injury and infarct size. Recent studies investigating neurotoxic mechanisms of COX-2 demonstrate both toxic and paradoxically protective effects of downstream prostaglandin receptor signaling pathways. We tested whether misoprostol, a PGE(2) receptor agonist that is utilized clinically as an anti-ulcer agent and signals through the protective PGE(2) EP2, EP3, and EP4 receptors, would reduce brain injury in the murine middle cerebral artery occlusion-reperfusion (MCAO-RP) model. Administration of misoprostol, at the time of MCAO or 2h after MCAO, resulted in significant rescue of infarct volume at 24 and 72h. Immunocytochemistry demonstrated dynamic regulation of the EP2 and EP4 receptors during reperfusion in neurons and endothelial cells of cerebral cortex and striatum, with limited expression of EP3 receptor. EP3-/- mice had no significant changes in infarct volume compared to control littermates. Moreover, administration of misoprostol to EP3+/+ and EP3-/- mice showed similar levels of infarct rescue, indicating that misoprostol protection was not mediated through the EP3 receptor. Taken together, these findings suggest a novel function for misoprostol as a protective agent in cerebral ischemia acting via the PGE(2) EP2 and/or EP4 receptors.

Does retirement reduce the risk of myocardial infarction?

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Olesen, Kasper; Rugulies, Reiner; Rod, Naja Hulvej

2014-01-01

BACKGROUND: Recent studies have suggested that retirement may have beneficial effects on health outcomes. In this study we examined whether the risk of myocardial infarction (MI) was reduced following retirement in a Danish population sample. METHODS: Participants were 617 511 Danish workers, born...... of 1.11 (95% confidence interval: 1.06, 1.16) when comparing retirees with active workers of the same age. CONCLUSIONS: This study does not support the hypothesis that retirement reduces risk of MI. On the contrary, we find that retirement is associated with a modestly increased risk of MI....

Asymmetry in the brain influenced the neurological deficits and infarction volume following the middle cerebral artery occlusion in rats

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Zhang Meizeng; Gao Huanmin

2008-01-01

Abstract Background Paw preference in rats is similar to human handedness, which may result from dominant hemisphere of rat brain. However, given that lateralization is the uniqueness of the humans, many researchers neglect the differences between the left and right hemispheres when selecting the middle cerebral artery occlusion (MCAO) in rats. The aim of this study was to evaluate the effect of ischemia in the dominant hemisphere on neurobehavioral function and on the cerebral infarction vol...

Effects of transcranial direct current stimulation on hemichannel pannexin-1 and neural plasticity in rat model of cerebral infarction.

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Jiang, T; Xu, R X; Zhang, A W; Di, W; Xiao, Z J; Miao, J Y; Luo, N; Fang, Y N

2012-12-13

The aim of this study was to investigate the effects of transcranial direct current stimulation (TDCS) on hemichannel pannexin-1 (PX1) in cortical neurons and neural plasticity, and explore the optimal time window of TDCS therapy after stroke. Adult male Sprague-Dawley rats (n=90) were randomly assigned to sham operation, middle cerebral artery occlusion (MCAO), and TDCS groups, and underwent sham operation, unilateral middle cerebral artery (MCA) electrocoagulation, and unilateral MCA electrocoagulation plus TDCS (daily anodal and cathodal 10 Hz, 0.1 mA TDCS for 30 min beginning day 1 after stroke), respectively. Motor function was assessed using the beam walking test (BWT), and density of dendritic spines (DS) and PX1 mRNA expression were compared among groups on days 3, 7, and 14 after stroke. Effects of PX1 blockage on DS in hippocampal neurons after hypoxia-ischemia were observed. TDCS significantly improved motor function on days 7 and 14 after stroke as indicated by reduced BWT scores compared with the MCAO group. The density of DS was decreased after stroke; the TDCS group had increased DS density compared with the MCAO group on days 3, 7, and 14 (all P<0.0001). Cerebral infarction induced increased PX1 mRNA expression on days 3, 7, and 14 (P<0.0001), and the peak PX1 mRNA expression was observed on day 7. TDCS did not decrease the up-regulated PX1 mRNA expression after stroke on day 3, but did reduce the increased post-stroke PX1 mRNA expression on days 7 and 14 (P<0.0001). TDCS increased the DS density after stroke, indicating that it may promote neural plasticity after stroke. TDCS intervention from day 7 to day 14 after stroke demonstrated motor function improvement and can down-regulate the elevated PX1 mRNA expression after stroke. Copyright © 2012 IBRO. Published by Elsevier Ltd. All rights reserved.

Inhibition of VEGF Signaling Reduces Diabetes-Exacerbated Brain Swelling, but Not Infarct Size, in Large Cerebral Infarction in Mice.

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Kim, Eunhee; Yang, Jiwon; Park, Keun Woo; Cho, Sunghee

2017-12-30

In light of repeated translational failures with preclinical neuroprotection-based strategies, this preclinical study reevaluates brain swelling as an important pathological event in diabetic stroke and investigates underlying mechanism of the comorbidity-enhanced brain edema formation. Type 2 (mild), type 1 (moderate), and mixed type 1/2 (severe) diabetic mice were subjected to transient focal ischemia. Infarct volume, brain swelling, and IgG extravasation were assessed at 3 days post-stroke. Expression of vascular endothelial growth factor (VEGF)-A, endothelial-specific molecule-1 (Esm1), and the VEGF receptor 2 (VEGFR2) was determined in the ischemic brain. Additionally, SU5416, a VEGFR2 inhibitor, was treated in the type 1/2 diabetic mice, and stroke outcomes were determined. All diabetic groups displayed bigger infarct volume and brain swelling compared to nondiabetic mice, and the increased swelling was disproportionately larger relative to infarct enlargement. Diabetic conditions significantly increased VEGF-A, Esm1, and VEGFR2 expressions in the ischemic brain compared to nondiabetic mice. Notably, in diabetic mice, VEGFR2 mRNA levels were positively correlated with brain swelling, but not with infarct volume. Treatment with SU5416 in diabetic mice significantly reduced brain swelling. The study shows that brain swelling is a predominant pathological event in diabetic stroke and that an underlying event for diabetes-enhanced brain swelling includes the activation of VEGF signaling. This study suggests consideration of stroke therapies aiming at primarily reducing brain swelling for subjects with diabetes.

Morphine Reduces Myocardial Infarct Size via Heat Shock Protein 90 in Rodents

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Bryce A. Small

2015-01-01

Full Text Available Opioids reduce injury from myocardial ischemia-reperfusion in humans. In experimental models, this mechanism involves GSK3β inhibition. HSP90 regulates mitochondrial protein import, with GSK3β inhibition increasing HSP90 mitochondrial content. Therefore, we determined whether morphine-induced cardioprotection is mediated by HSP90 and if the protective effect is downstream of GSK3β inhibition. Male Sprague-Dawley rats, aged 8–10 weeks, were subjected to an in vivo myocardial ischemia-reperfusion injury protocol involving 30 minutes of ischemia followed by 2 hours of reperfusion. Hemodynamics were continually monitored and myocardial infarct size determined. Rats received morphine (0.3 mg/kg, the GSK3β inhibitor, SB216763 (0.6 mg/kg, or saline, 10 minutes prior to ischemia. Some rats received selective HSP90 inhibitors, radicicol (0.3 mg/kg, or deoxyspergualin (DSG, 0.6 mg/kg alone or 5 minutes prior to morphine or SB216763. Morphine reduced myocardial infarct size when compared to control (42 ± 2% versus 60 ± 1%. This protection was abolished by prior treatment of radicicol or DSG (59 ± 1%, 56 ± 2%. GSK3β inhibition also reduced myocardial infarct size (41 ± 2% with HSP90 inhibition by radicicol or DSG partially inhibiting SB216763-induced infarct size reduction (54 ± 3%, 47 ± 1%, resp.. These data suggest that opioid-induced cardioprotection is mediated by HSP90. Part of this protection afforded by HSP90 is downstream of GSK3β, potentially via the HSP-TOM mitochondrial import pathway.

  Adenosine-diphosphate (ADP) reduces infarct size and improves porcine heart function after myocardial infarction

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Bune, Laurids Touborg; Larsen, Jens Kjærgaard Rolighed; Thaning, Pia

2013-01-01

Acute myocardial infarction continues to be a major cause of morbidity and mortality. Timely reperfusion can substantially improve outcomes and the administration of cardioprotective substances during reperfusion is therefore highly attractive. Adenosine diphosphate (ADP) and uridine-5-triphoshat...... infusion during reperfusion reduces IS by ~20% independently from systemic release of t-PA. ADP-induced reduction in both preload and afterload could account for the beneficial myocardial effect....

UTP reduces infarct size and improves mice heart function after myocardial infarct via P2Y2 receptor

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Cohen, A; Shainberg, Asher; Hochhauser, E

2011-01-01

Pyrimidine nucleotides are signaling molecules, which activate G protein-coupled membrane receptors of the P2Y family. P2Y(2) and P2Y(4) receptors are part of the P2Y family, which is composed of 8 subtypes that have been cloned and functionally defined. We have previously found that uridine-5......'-triphosphate (UTP) reduces infarct size and improves cardiac function following myocardial infarct (MI). The aim of the present study was to determine the role of P2Y(2) receptor in cardiac protection following MI using knockout (KO) mice, in vivo and wild type (WT) for controls. In both experimental groups...... used (WT and P2Y(2)(-/-) receptor KO mice) there were 3 subgroups: sham, MI, and MI+UTP. 24h post MI we performed echocardiography and measured infarct size using triphenyl tetrazolium chloride (TTC) staining on all mice. Fractional shortening (FS) was higher in WT UTP-treated mice than the MI group...

Protection by the gross saponins of Tribulus terrestris against cerebral ischemic injury in rats involves the NF-κB pathway

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En-ping Jiang

2011-06-01

Full Text Available The aim of this study was to investigate whether the gross saponins of Tribulus terrestris (GSTT, a traditional Chinese herbal medicine, have neuroprotective effects on rats subjected to middle cerebral artery occlusion (MCAO, through nuclear factor-κB (NF-κB pathway and inflammatory mediators. Cerebral ischemia was produced by MCAO in either untreated (control or GSTT-pretreated rats, and the animals were examined for infarct volume, cerebral edema, neuro-behavioral abnormality and pathological changes. Meanwhile, the expression of NF-κB protein in brain tissue was analyzed on Western blots and the serum levels of TNF-α and IL-1 were determined by ELISA. The experimental results demonstrated that, compared with the control MCAO group, GSTT-pretreated MCAO group had significantly reduced infarct volume, brain edema and neuro-behavioral abnormality, and lesser degree of pathologic changes in the brain, as well as had lower levels of serum TNF-α and IL-1β, and higher levels of brain NF-κB (P<0.05. Furthermore, treatment with an NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC abolished the protective effects of GSTT against MCAO-induced cerebral ischemic injury. These results indicated that GSTT's ability to protect against cerebral ischemic injury was mediated through the NF-κB signaling pathway, and that GSTT may act through inhibition of the production of inflammatory mediators.

Chronic Metformin Treatment is Associated with Reduced Myocardial Infarct Size in Diabetic Patients with ST-segment Elevation Myocardial Infarction

NARCIS (Netherlands)

Lexis, Chris P. H.; Wieringa, Wouter G.; Hiemstra, Bart; van Deursen, Vincent M.; Lipsic, Erik; van der Harst, Pim; van Veldhuisen, Dirk J.; van der Horst, Iwan C. C.

Increased myocardial infarct (MI) size is associated with higher risk of developing left ventricular dysfunction, heart failure and mortality. Experimental studies have suggested that metformin treatment reduces MI size after induced ischaemia but human data is lacking. We aimed to investigate the

Neuroprotective effect of STAZN, a novel azulenyl nitrone antioxidant, in focal cerebral ischemia in rats: dose-response and therapeutic window

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Ley, James J.; Belayev, Ludmila; Saul, Isabel; Becker, David A.; Ginsberg., Myron D.

2007-01-01

Stilbazulenyl nitrone (STAZN) is a potent antioxidant that, in a rat model of transient focal cerebral ischemia, confers significant enduring functional and morphological neuroprotection. This study investigated the influence of dose and time of administration on the neuroprotective effects of STAZN in the intraluminal-suture model of middle cerebral artery occlusion (MCAo). Dose-Response At 2 and 4h after the onset of MCAo, animals received intravenously either STAZN (low dose=0.07 mg/kg, n=8), (medium dose=0.7 mg/kg, n=9), (high dose=3.5 mg/kg, n=9), an equivalent volume of vehicle (30% Solutol HS15 and 70% isotonic saline, 0.37 ml/kg, n=5), or saline (0.37 ml/kg, n=5). Only the medium dose improved scores (p<0.05) on a standardized neurobehavioral test at 1, 2 and 3d after MCAo. Only the medium dose reduced the total infarction (51%, p=0.014) compared to controls. These results indicate that STAZN exhibits maximal neuroprotection at the 0.7 mg/kg dose. Therapeutic Window STAZN (0.6 mg/kg) dissolved in dimethylsulfoxide was given intra-peritoneally at 2 and 4h (n=11), 3 and 5h (n=10), 4 and 6h (n=10), or 5 and 7h (n=7) after the onset of MCAo. Additional doses were given at 24 and 48h. Vehicle (dimethylsulfoxide, 2.0 ml/kg, n=6) was administered at 3, 5, 24 and 48h. STAZN treatment initiated at 2 or 3h after the onset of MCAo improved neurological scores (p<0.001) and reduced total infarction (42.2%, p<0.05) compared to controls. PMID:17945201

Cyclosporine A at reperfusion fails to reduce infarct size in the in vivo rat heart.

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De Paulis, Damien; Chiari, Pascal; Teixeira, Geoffrey; Couture-Lepetit, Elisabeth; Abrial, Maryline; Argaud, Laurent; Gharib, Abdallah; Ovize, Michel

2013-09-01

We examined the effects on infarct size and mitochondrial function of ischemic (Isch), cyclosporine A (CsA) and isoflurane (Iso) preconditioning and postconditioning in the in vivo rat model. Anesthetized open-chest rats underwent 30 min of ischemia followed by either 120 min (protocol 1: infarct size assessment) or 15 min of reperfusion (protocol 2: assessment of mitochondrial function). All treatments administered before the 30-min ischemia (Pre-Isch, Pre-CsA, Pre-Iso) significantly reduced infarct as compared to control. In contrast, only Post-Iso significantly reduced infarct size, while Post-Isch and Post-CsA had no significant protective effect. As for the postconditioning-like interventions, the mitochondrial calcium retention capacity significantly increased only in the Post-Iso group (+58 % vs control) after succinate activation. Only Post-Iso increased state 3 (+177 and +62 %, for G/M and succinate, respectively) when compared to control. Also, Post-Iso reduced the hydrogen peroxide (H2O2) production (-46 % vs control) after complex I activation. This study suggests that isoflurane, but not cyclosporine A, can prevent lethal reperfusion injury in this in vivo rat model. This might be related to the need for a combined effect on cyclophilin D and complex I during the first minutes of reperfusion.

Nylon filament coated with paraffin for intraluminal permanent middle cerebral artery occlusion in rats.

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Zuo, Xia-Lin; Wu, Ping; Ji, Ai-Min

2012-06-21

A variety of intraluminal nylon filament has been used in rat middle cerebral artery occlusion (MCAO) models. However the lesion extent and its reproducibility vary among laboratories. The properties of nylon filament play a part of reasons for these variations. In the present study, we used paraffin-coated nylon filament for rat MCAO model, tested the effects and advanced improvement for making the rat MCAO. Forty male Sprague-Dawley (SD) rats were randomized into two groups, MCAO with traditional uncoated nylon filament (uMCAO) and MCAO with paraffin-coated nylon filament (cMCAO), three rats as normal group and sham group respectively. Assessment included mortality rates, model success rates, neurological deficit evaluation, and infarct volume. The study showed two rats died in uMCAO group, no rat died in cMCAO group within the 12h. The model success rate of uMCAO was 100%, while the uMCAO group was 55% (n=20, two died within 12h, seven rats were excluded as the brain slices showed no TTC staining due to subarachanoid hemorrhage). Neurological evaluation demonstrated group cMCAO had more worse neurological outcomes than group uMCAO, and the difference was statistically signification (pparaffin-coated nylon filament intraluminal occlusion provide better occlusion of middle cerebral artery than the uncoated nylon filament, improve the consistent of model, and raise the success rate to reduce the number of experimental animals. These positive results are much encouraging and interesting. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

Identification of ischemic regions in a rat model of stroke.

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Popp, Anke; Jaenisch, Nadine; Witte, Otto W; Frahm, Christiane

2009-01-01

Investigations following stroke first of all require information about the spatio-temporal dimension of the ischemic core as well as of perilesional and remote affected tissue. Here we systematically evaluated regions differently impaired by focal ischemia. Wistar rats underwent a transient 30 or 120 min suture-occlusion of the middle cerebral artery (MCAO) followed by various reperfusion times (2 h, 1 d, 7 d, 30 d) or a permanent MCAO (1 d survival). Brains were characterized by TTC, thionine, and immunohistochemistry using MAP2, HSP72, and HSP27. TTC staining reliably identifies the infarct core at 1 d of reperfusion after 30 min MCAO and at all investigated times following 120 min and permanent MCAO. Nissl histology denotes the infarct core from 2 h up to 30 d after transient as well as permanent MCAO. Absent and attenuated MAP2 staining clearly identifies the infarct core and perilesional affected regions at all investigated times, respectively. HSP72 denotes perilesional areas in a limited post-ischemic time (1 d). HSP27 detects perilesional and remote impaired tissue from post-ischemic day 1 on. Furthermore a simultaneous expression of HSP72 and HSP27 in perilesional neurons was revealed. TTC and Nissl staining can be applied to designate the infarct core. MAP2, HSP72, and HSP27 are excellent markers not only to identify perilesional and remote areas but also to discriminate affected neuronal and glial populations. Moreover markers vary in their confinement to different reperfusion times. The extent and consistency of infarcts increase with prolonged occlusion of the MCA. Therefore interindividual infarct dimension should be precisely assessed by the combined use of different markers as described in this study.

Limb Remote Ischemic Postconditioning Reduces Ischemia-Reperfusion Injury by Inhibiting NADPH Oxidase Activation and MyD88-TRAF6-P38MAP-Kinase Pathway of Neutrophils

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Gangling Chen

2016-11-01

Full Text Available Limb remote ischemic postconditioning (LRIP has been confirmed to reduce the ischemia-reperfusion injury but its mechanisms are still not clear. This study clarified the mechanism of LRIP based on the nicotinamide-adenine dinucleotide phosphate (NADPH oxidase and Myeloid differentiation factor 88 (MyD88-Tumor necrosis factor (TNF receptor-associated factor 6 (TRAF6-P38 pathway of neutrophils. Rat middle cerebral artery occlusion (MCAO model was used in this study. Ischemia-reperfusion injury was carried out by MCAO 1.5 h followed by 24 h reperfusion. LRIP operation was performed to the left femoral artery at 0, 1 or 3 h after reperfusion. Behavioral testing, including postural reflex test, vibrissae-elicited forelimb placing test and tail hang test, showed that LRIP operated at 0 h of reperfusion could significantly ameliorate these behavioral scores. Pathological examinations, infarct size, Myeloperoxidase (MPO activity showed that LRIP operated at 0 h of reperfusion could significantly ameliorate the pathological scores, reduce the infarct size and MPO activity in the brain and increase the MPO activity in the left leg. By using Neutrophil counting, immunofluorescence and real-time PCR techniques, we found that LRIP operated at 0 h of reperfusion could reduce neutrophil counts in the peripheral blood and downregulate the activation of neutrophil in the peripheral blood and rat brain. Western blots revealed that MyD88, TRAF6, p38 mitogen-activated protein kinase (p38-MAPK in neutrophils and the phosphorylation of p47phox (Ser 304 and Ser 345 in neutrophil could be downregulated by LRIP. Our study suggests that LRIP inhibits the number and activation of neutrophils in the rat brain and peripheral blood linked to down-regulating the activation of NADPH oxidase in neutrophils by MyD88/TRAF6/p38-MAPK pathway.

Neuroprotective effects of andrographolide in a rat model of permanent cerebral ischaemia

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Chan, Su Jing; Wong, WS Fred; Wong, Peter TH; Bian, Jin-Song

2010-01-01

BACKGROUND AND PURPOSE Andrographolide is a diterpenoid lactone isolated from a traditional medicinal herb, Andrographis paniculata. It possesses potent anti-inflammatory activity. The present study examined potential therapeutic effects of andrographolide on cerebral ischaemia using a rat model with permanent middle cerebral artery occlusion (pMCAO). EXPERIMENTAL APPROACH The MCA in rats was permanently occluded (by cautery), and 24 h later neurological effects were assessed with behavioural scores. Infarct volume and microglial activation were determined histologically. The p65 form of the transcription factor, nuclear factor-κB (NF-κB), was measured by Western blot, and cytokines by immunoassay of brain extracts. KEY RESULTS Andrographolide, given i.p. 1 h after pMCAO, reduced infarct volume with a maximum reduction of approximately 50% obtained at 0.1 mg·kg−1. Neurological deficits were also reduced by andrographolide, reflecting a correlation between infarct volume and neurological deficits. pMCAO was found to induce activation of microglia and elevate tumour necrosis factor (TNF)-α, interleukin (IL)-1β and prostaglandin (PG)E2 in the ischaemic brain areas. Andrographolide (0.1 mg·kg−1) significantly attenuated or abolished these effects. In addition, andrographolide suppressed the translocation of p65 from cytosol to nucleus, indicating reduced NF-κB activation. CONCLUSIONS AND IMPLICATIONS Andrographolide exhibited neuroprotective effects, with accompanying suppression of NF-κB and microglial activation, and reduction in the production of cytokines including TNF-α and IL-1β, and pro-inflammatory factors such as PGE2. Our findings suggest that andrographolide may have therapeutic value in the treatment of stroke. PMID:20880404

Prodigiosin inhibits gp91phox and iNOS expression to protect mice against the oxidative/nitrosative brain injury induced by hypoxia–ischemia

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Chang, Chia-Che; Wang, Yea-Hwey; Chern, Chang-Ming; Liou, Kuo-Tong; Hou, Yu-Chang; Peng, Yu-Ta; Shen, Yuh-Chiang

2011-01-01

This study aimed to explore the mechanisms by which prodigiosin protects against hypoxia-induced oxidative/nitrosative brain injury induced by middle cerebral artery occlusion/reperfusion (MCAo/r) injury in mice. Hypoxia in vitro was modeled using oxygen–glucose deprivation (OGD) followed by reoxygenation of BV-2 microglial cells. Our results showed that treatment of mice that have undergone MCAo/r injury with prodigiosin (10 and 100 μg/kg, i.v.) at 1 h after hypoxia ameliorated MCAo/r-induced oxidative/nitrosative stress, brain infarction, and neurological deficits in the mice, and enhanced their survival rate. MCAo/r induced a remarkable production in the mouse brains of reactive oxygen species (ROS) and a significant increase in protein nitrosylation; this primarily resulted from enhanced expression of NADPH oxidase 2 (gp91 phox ), inducible nitric oxide synthase (iNOS), and the infiltration of CD11b leukocytes due to breakdown of blood–brain barrier (BBB) by activation of nuclear factor-kappa B (NF-κB). All these changes were significantly diminished by prodigiosin. In BV-2 cells, OGD induced ROS and nitric oxide production by up-regulating gp91 phox and iNOS via activation of the NF-κB pathway, and these changes were suppressed by prodigiosin. In conclusion, our results indicate that prodigiosin reduces gp91 phox and iNOS expression possibly by impairing NF-κB activation. This compromises the activation of microglial and/or inflammatory cells, which then, in turn, mediates prodigiosin's protective effect in the MCAo/r mice. -- Highlights: ► Prodigiosin ameliorated brain infarction and deficits. ► Prodigiosin protected against hypoxia/reperfusion-induced brain injury. ► Prodigiosin diminished oxidative/nitrosativestress and leukocytes infiltration. ► Prodigiosin reduced BBB breakdown. ► Prodigiosin down-regulated gp91 phox and iNOS by inhibiting NF-κB activation.

Neuroprotective Effect of Xueshuantong for Injection (Lyophilized in Transient and Permanent Rat Cerebral Ischemia Model

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Xumei Wang

2015-01-01

Full Text Available Xueshuantong for Injection (Lyophilized (XST, a Chinese Materia Medica standardized product extracted from Panax notoginseng (Burk., is used extensively for the treatment of cerebrovascular diseases such as acutely cerebral infarction clinically in China. In the present study, we evaluated the acute and extended protective effects of XST in different rat cerebral ischemic model and explored its effect on peroxiredoxin (Prx 6-toll-like receptor (TLR 4 signaling pathway. We found that XST treatment for 3 days could significantly inhibit transient middle cerebral artery occlusion (MCAO induced infarct volume and swelling percent and regulate the mRNA expression of interleukin-1β (IL-1β, IL-17, IL-23p19, tumor necrosis factor-α (TNFα, and inducible nitric oxide synthase (iNOS in brain. Further study demonstrated that treatment with XST suppressed the protein expression of peroxiredoxin (Prx 6-toll-like receptor (TLR 4 and phosphorylation level of p38 and upregulated the phosphorylation level of STAT3. In permanent MCAO rats, XST could reduce the infarct volume and swelling percent. Moreover, our results revealed that XST treatment could increase the rats’ weight and improve a batch of functional outcomes. In conclusion, the present data suggested that XST could protect against ischemia injury in transient and permanent MCAO rats, which might be related to Prx6-TLR4 pathway.

Neuroprotective Efficacy of an Aminopropyl Carbazole Derivative P7C3-A20 in Ischemic Stroke.

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Wang, Shu-Na; Xu, Tian-Ying; Wang, Xia; Guan, Yun-Feng; Zhang, Sai-Long; Wang, Pei; Miao, Chao-Yu

2016-09-01

NAMPT is a novel therapeutic target of ischemic stroke. The aim of this study was to investigate the effect of a potential NAMPT activator, P7C3-A20, an aminopropyl carbazole derivative, on ischemic stroke. In vitro study, neuron protection effect of P7C3-A20 was investigated by co-incubation with primary neurons subjected to oxygen-glucose deprivation (OGD) or oxygen-glucose deprivation/reperfusion (OGD/R) injury. In vivo experiment, P7C3-A20 was administrated in middle cerebral artery occlusion (MCAO) rats and infarct volume was examined. Lastly, the brain tissue nicotinamide adenine dinucleotide (NAD) levels were detected in P7C3-A20 treated normal or MCAO mice. Cell viability, morphology, and Tuj-1 staining confirmed the neuroprotective effect of P7C3-A20 in OGD or OGD/R model. P7C3-A20 administration significantly reduced cerebral infarction in MCAO rats. Moreover, brain NAD levels were elevated both in normal and MCAO mice after P7C3-A20 treatment. P7C3-A20 has neuroprotective effect in cerebral ischemia. The study contributes to the development of NAMPT activators against ischemic stroke and expands the horizon of the neuroprotective effect of aminopropyl carbazole chemicals. © 2016 John Wiley & Sons Ltd.

Membrane attack complex inhibitor CD59a protects against focal cerebral ischemia in mice

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Nietfeld Wilfried

2010-03-01

Full Text Available Abstract Background The complement system is a crucial mediator of inflammation and cell lysis after cerebral ischemia. However, there is little information about the exact contribution of the membrane attack complex (MAC and its inhibitor-protein CD59. Methods Transient focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO in young male and female CD59a knockout and wild-type mice. Two models of MCAO were applied: 60 min MCAO and 48 h reperfusion, as well as 30 min MCAO and 72 h reperfusion. CD59a knockout animals were compared to wild-type animals in terms of infarct size, edema, neurological deficit, and cell death. Results and Discussion CD59a-deficiency in male mice caused significantly increased infarct volumes and brain swelling when compared to wild-type mice at 72 h after 30 min-occlusion time, whereas no significant difference was observed after 1 h-MCAO. Moreover, CD59a-deficient mice had impaired neurological function when compared to wild-type mice after 30 min MCAO. Conclusion We conclude that CD59a protects against ischemic brain damage, but depending on the gender and the stroke model used.

Docosahexaenoic acid signaling modulates cell survival in experimental ischemic stroke penumbra and initiates long-term repair in young and aged rats.

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Tiffany N Eady

Full Text Available Docosahexaenoic acid, a major omega-3 essential fatty acid family member, improves behavioral deficit and reduces infarct volume and edema after experimental focal cerebral ischemia. We hypothesize that DHA elicits neuroprotection by inducing AKT/p70S6K phosphorylation, which in turn leads to cell survival and protects against ischemic stroke in young and aged rats.Rats underwent 2 h of middle cerebral artery occlusion (MCAo. DHA, neuroprotectin D1 (NPD1 or vehicle (saline was administered 3 h after onset of stroke. Neurological function was evaluated on days 1, 2, 3, and 7. DHA treatment improved functional recovery and reduced cortical, subcortical and total infarct volumes 7 days after stroke. DHA also reduced microglia infiltration and increased the number of astrocytes and neurons when compared to vehicle on days 1 and 7. Increases in p473 AKT and p308 AKT phosphorylation/activation were observed in animals treated with DHA 4 h after MCAo. Activation of other members of the AKT signaling pathway were also observed in DHA treated animals including increases in pS6 at 4 h and pGSK at 24 h. DHA or NPD1 remarkably reduced total and cortical infarct in aged rats. Moreover, we show that in young and aged rats DHA treatment after MCAo potentiates NPD1 biosynthesis. The phosphorylation of p308 AKT or pGSK was not different between groups in aged rats. However, pS6 expression was increased with DHA or NPD1 treatment when compared to vehicle.We suggest that DHA induces cell survival, modulates the neuroinflammatory response and triggers long term restoration of synaptic circuits. Both DHA and NPD1 elicited remarkable protection in aged animals. Accordingly, activation of DHA signaling might provide benefits in the management of ischemic stroke both acutely as well as long term to limit ensuing disabilities.

The Protective Effect of Human Umbilical Cord Blood CD34+ Cells and Estradiol against Focal Cerebral Ischemia in Female Ovariectomized Rat: Cerebral MR Imaging and Immunohistochemical Study.

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Ching-Chung Liang

Full Text Available Human umbilical cord blood derived CD34+ stem cells are reported to mediate therapeutic effects in stroke animal models. Estrogen was known to protect against ischemic injury. The present study wished to investigate whether the protective effect of CD34+ cells against ischemic injury can be reinforced with complemental estradiol treatment in female ovariectomized rat and its possible mechanism. Experiment 1 was to determine the best optimal timing of CD34+ cell treatment for the neuroprotective effect after 60-min middle cerebral artery occlusion (MCAO. Experiment 2 was to evaluate the adjuvant effect of 17β-estradiol on CD34+ cell neuroprotection after MCAO. Experiment 1 showed intravenous infusion with CD34+ cells before MCAO (pre-treatment caused less infarction size than those infused after MCAO (post-treatment on 7T magnetic resonance T2-weighted images. Experiment 2 revealed infarction size was most significantly reduced after CD34+ + estradiol pre-treatment. When compared with no treatment group, CD34+ + estradiol pre-treatment showed significantly less ADC reduction at 2 h and 2 d, less CBF reduction at 2 h and less hyperperfusion at 2 d. The immunoreactivity of c-Fos, c-Jun and GFAP was attenuated, and BDNF showed significant recovery from 2 h to 2 d after MCAO, especially after CD34+ + estradiol pre-treatment. The present study suggests pre-treatment with CD34+ cells with complemental estradiol can be most protective against ischemic injury, which may act through stabilization of cerebral hemodynamics and normalization of the expressions of immediate early genes and BDNF.

Intraoperative laser speckle contrast imaging improves the stability of rodent middle cerebral artery occlusion model

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Yuan, Lu; Li, Yao; Li, Hangdao; Lu, Hongyang; Tong, Shanbao

2015-09-01

Rodent middle cerebral artery occlusion (MCAO) model is commonly used in stroke research. Creating a stable infarct volume has always been challenging for technicians due to the variances of animal anatomy and surgical operations. The depth of filament suture advancement strongly influences the infarct volume as well. We investigated the cerebral blood flow (CBF) changes in the affected cortex using laser speckle contrast imaging when advancing suture during MCAO surgery. The relative CBF drop area (CBF50, i.e., the percentage area with CBF less than 50% of the baseline) showed an increase from 20.9% to 69.1% when the insertion depth increased from 1.6 to 1.8 cm. Using the real-time CBF50 marker to guide suture insertion during the surgery, our animal experiments showed that intraoperative CBF-guided surgery could significantly improve the stability of MCAO with a more consistent infarct volume and less mortality.

Additive Neuroprotective Effect of Borneol with Mesenchymal Stem Cells on Ischemic Stroke in Mice

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Xiao-Guang Zhang

2018-01-01

Full Text Available Intravenous stem cell transplantation initiates neuroprotection related to the secretion of trophic factor. Borneol, a potential herbal neuroprotective agent, is a penetration enhancer. Here, we aimed to investigate whether they have additive neuroprotective effect on cerebral ischemia. Borneol was given to mice by gavage 3 days before middle cerebral artery occlusion (MCAO induction until the day when the mice were sacrificed. Mesenchymal stem cells (MSCs were intravenously injected at 24 h after MCAO induction. Neurological deficits, infarct volume, cell death, and neurogenesis were evaluated. Combined use of MSCs and borneol could more effectively reduce infarction volume and cell apoptosis, enhance neurogenesis, and improve the functional recovery than that of MSCs alone. The findings showed that combined use of borneol and stem cells provided additive neuroprotective effect on cerebral ischemia. However, the supposed effect of borneol on the improved MSC penetration still needs further direct evidence.

Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats

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I. Stefanon

2009-10-01

Full Text Available Myocardial infarction leads to compensatory ventricular remodeling. Disturbances in myocardial contractility depend on the active transport of Ca2+ and Na+, which are regulated by Na+-K+ ATPase. Inappropriate regulation of Na+-K+ ATPase activity leads to excessive loss of K+ and gain of Na+ by the cell. We determined the participation of Na+-K+ ATPase in ventricular performance early and late after myocardial infarction. Wistar rats (8-10 per group underwent left coronary artery ligation (infarcted, Inf or sham-operation (Sham. Ventricular performance was measured at 3 and 30 days after surgery using the Langendorff technique. Left ventricular systolic pressure was obtained under different ventricular diastolic pressures and increased extracellular Ca2+ concentrations (Ca2+e and after low and high ouabain concentrations. The baseline coronary perfusion pressure increased 3 days after myocardial infarction and normalized by 30 days (Sham 3 = 88 ± 6; Inf 3 = 130 ± 9; Inf 30 = 92 ± 7 mmHg; P < 0.05. The inotropic response to Ca2+e and ouabain was reduced at 3 and 30 days after myocardial infarction (Ca2+ = 1.25 mM; Sham 3 = 70 ± 3; Inf 3 = 45 ± 2; Inf 30 = 29 ± 3 mmHg; P < 0.05, while the Frank-Starling mechanism was preserved. At 3 and 30 days after myocardial infarction, ventricular Na+-K+ ATPase activity and contractility were reduced. This Na+-K+ ATPase hypoactivity may modify the Na+, K+ and Ca2+ transport across the sarcolemma resulting in ventricular dysfunction.

Statins reduce new-onset atrial fibrillation in a first-time myocardial infarction population

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Bang, Casper N; Gislason, Gunnar H; Greve, Anders M

2014-01-01

AIM: To evaluate the effect of statins on reducing new-onset atrial fibrillation (AF) in a large real-world post-myocardial infarction (MI) population. Subsequently, to test if different statin doses, various types and compliance affected the incidence of new-onset AF post MI. METHODS: All patients...

Neuroprotection of taurine through inhibition of 12/15 lipoxygenase pathway in cerebral ischemia of rats.

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Zhang, Zhe; Yu, Rongbo; Cao, Lei

2017-05-01

Cerebral ischemia exhibits a multiplicity of pathophysiological mechanisms. Taurine (Tau), an endogenous substance, possesses a number of cytoprotective properties. The aim of the present study was to examine the neuroprotective effect of Tau, through affecting 12/15 lipoxygenase (12/15-LOX) signal pathway in an acute permanent middle cerebral artery occlusion (MCAO) model of rats. Sprague-Dawley rats were randomly divided into 3 groups (n = 10), namely the sham-operated group, MCAO group and Tau group. Tau was intraperitoneally administrated immediately after cerebral ischemia. At 24 h after MCAO, neurological function score, brain water content and infarct volume were assessed. The expression of 12/15-lipoxygenase (12/15-LOX), p38 mitogen-activated protein kinase (p38 MAPK), and cytosolic phospholipase A2 (cPLA2) was measured by Western blot. Enzyme-linked immunosorbent assay was used to evaluate the inflammatory factors TNF-α, IL-1β and IL-6 in serum. Compared with MCAO group, taurine significantly improved neurological function and significantly reduced brain water content (p Taurine protected the brain from damage caused by MCAO; this effect may be through down-regulation of 12/15-LOX, p38 MAPK, and cPLA2.

RESVERATROL PRECONDITIONING INDUCES A NOVEL EXTENDED WINDOW OF ISCHEMIC TOLERANCE IN THE MOUSE BRAIN

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Koronowski, Kevin B.; Dave, Kunjan R.; Saul, Isabel; Camarena, Vladimir; Thompson, John W.; Neumann, Jake T.; Young, Juan I.; Perez-Pinzon, Miguel A.

2015-01-01

Background and Purpose Prophylactic treatments that afford neuroprotection against stroke may emerge from the field of preconditioning. Resveratrol mimics ischemic preconditioning, reducing ischemic brain injury when administered two days prior to global ischemia in rats. This protection is linked to Sirt1 and enhanced mitochondrial function possibly through its repression of UCP2. BDNF is another neuroprotective protein associated with Sirt1. In this study we sought to identify the conditions of resveratrol preconditioning (RPC) that most robustly induce neuroprotection against focal ischemia in mice. Methods We tested four different RPC paradigms against a middle cerebral artery occlusion (MCAo) model of stroke. Infarct volume and neurological score were calculated 24 hours following MCAo. Sirt1-chromatin binding was evaluated by ChIP-qPCR. Percoll gradients were used to isolate synaptic fractions and changes in protein expression were determined via Western blot analysis. BDNF concentration was measured using a BDNF-specific ELISA assay. Results While repetitive RPC induced neuroprotection from MCAo, strikingly one application of RPC 14 days prior to MCAo showed the most robust protection, reducing infarct volume by 33% and improving neurological score by 28%. Fourteen days following RPC, Sirt1 protein was increased 1.5 fold and differentially bound to the UCP2 and BDNF promoter regions. Accordingly, synaptic UCP2 protein decreased by 23% and cortical BDNF concentration increased 26%. Conclusions RPC induces a novel extended window of ischemic tolerance in the brain that lasts for at least 14 days. Our data suggest that this tolerance may be mediated by Sirt1, through upregulation of BDNF and downregulation of UCP2. PMID:26159789

[Study of neuron-protective effect and mechanism of neuregulin1β against cerebral ischemia reperfusion-induced injury in rats].

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Ji, Y Q; Zhang, R; Teng, L; Li, H Y; Guo, Y L

2017-07-18

Objective: Thecurrent study is to explore the neuron-protective mechanism of neuregulin1β (NRG1β) in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) through inhibiting the c-Jun phosphorylation. Methods: After 24 h of MCAO/R (referring to Longa's method), neurobehavioral function was measured by modified neurological severity score (mNSS) test; the cerebral infarction volume was detected by triphenyltetrazolium chloride (TTC) staining; the blood brain barrier (BBB) permeability was measured by Evans Blue (EB); the neuron morphology of brain tissue was observed by Nissl stain; the ultra-structures of the neurons were observed by transmission electron microscopy (TEM); the apoptotic neurons were counted by in situ cell death detection kit colocalized with NeuN; the expressions of phospho-c-Jun was determined by immunofluorescent labeling and Western blot analysis. Results: Compared with the sham-operation rats, the rats receiving MCAO/R showed increased mNSS (9.7±1.2), cerebral infarction volume (41.4±3.0)%, permeability of BBB, deformation of neurons, ischemia-induced apoptosis (0.63±0.04), and enhanced expression of phospho-c-Jun protein (0.90±0.07) (all P <0.05). Our data indicated that NRG1β attenuated neurologic deficits (6.4±0.9), decreased the cerebral infarction volume (10.4±0.5), reduced EB extravasation (1.55±0.13) and the deformation of neurons, protected the ultra-structure of neurons, blocked ischemia-induced apoptosis (0.23±0.02), through down-regulated phospho-c-Jun expression (0.40±0.03) in MCAO/R rats ( P <0.05). Conclusion: NRG1β exerts neuron-protective effects against ischemia reperfusion-induced injury in rats through inhibiting the c-Jun phosphorylation.

Neuronal precursor cell proliferation in the hippocampus after transient cerebral ischemia: a comparative study of two rat strains using stereological tools.

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Kelsen, Jesper; Larsen, Marianne H; Sørensen, Jens Christian; Møller, Arne; Frøkiaer, Jørgen; Nielsen, Søren; Nyengaard, Jens R; Mikkelsen, Jens D; Rønn, Lars Christian B

2010-04-06

We are currently investigating microglial activation and neuronal precursor cell (NPC) proliferation after transient middle cerebral artery occlusion (tMCAo) in rats. This study aimed: (1) to investigate differences in hippocampal NPC proliferation in outbred male spontaneously hypertensive rats (SHRs) and Sprague-Dawley rats (SDs) one week after tMCAo; (2) to present the practical use of the optical fractionator and 2D nucleator in stereological brain tissue analyses; and (3) to report our experiences with an intraluminal tMCAo model where the occluding filament is advanced 22 mm beyond the carotid bifurcation and the common carotid artery is clamped during tMCAo. Twenty-three SDs and twenty SHRs were randomized into four groups subjected to 90 minutes tMCAo or sham. BrdU (50 mg/kg) was administered intraperitoneally twice daily on Day 4 to 7 after surgery. On Day 8 all animals were euthanized. NeuN-stained tissue sections were used for brain and infarct volume estimation with the 2D nucleator and Cavalieri principle. Brains were studied for the presence of activated microglia (ED-1) and hippocampal BrdU incorporation using the optical fractionator. We found no significant difference or increase in post-ischemic NPC proliferation between the two strains. However, the response to remote ischemia may differ between SDs and SHRs. In three animals increased post-stroke NPC proliferation was associated with hippocampal ischemic injury. The mean infarct volume was 89.2 +/- 76.1 mm3 in SHRs and 16.9 +/- 22.7 mm3 in SDs (p < 0.005). Eight out of eleven SHRs had ischemic neocortical damage in contrast to only one out of 12 SDs. We observed involvement of the anterior choroidal and hypothalamic arteries in several animals from both strains and the anterior cerebral artery in two SHRs. We found no evidence of an early hippocampal NPC proliferation one week after tMCAo in both strains. Infarction within the anterior choroidal artery could induce hippocampal ischemia and

Reliability of infarct volumetry: Its relevance and the improvement by a software-assisted approach.

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Friedländer, Felix; Bohmann, Ferdinand; Brunkhorst, Max; Chae, Ju-Hee; Devraj, Kavi; Köhler, Yvette; Kraft, Peter; Kuhn, Hannah; Lucaciu, Alexandra; Luger, Sebastian; Pfeilschifter, Waltraud; Sadler, Rebecca; Liesz, Arthur; Scholtyschik, Karolina; Stolz, Leonie; Vutukuri, Rajkumar; Brunkhorst, Robert

2017-08-01

Despite the efficacy of neuroprotective approaches in animal models of stroke, their translation has so far failed from bench to bedside. One reason is presumed to be a low quality of preclinical study design, leading to bias and a low a priori power. In this study, we propose that the key read-out of experimental stroke studies, the volume of the ischemic damage as commonly measured by free-handed planimetry of TTC-stained brain sections, is subject to an unrecognized low inter-rater and test-retest reliability with strong implications for statistical power and bias. As an alternative approach, we suggest a simple, open-source, software-assisted method, taking advantage of automatic-thresholding techniques. The validity and the improvement of reliability by an automated method to tMCAO infarct volumetry are demonstrated. In addition, we show the probable consequences of increased reliability for precision, p-values, effect inflation, and power calculation, exemplified by a systematic analysis of experimental stroke studies published in the year 2015. Our study reveals an underappreciated quality problem in translational stroke research and suggests that software-assisted infarct volumetry might help to improve reproducibility and therefore the robustness of bench to bedside translation.

High-density lipoprotein-based therapy reduces the hemorrhagic complications associated with tissue plasminogen activator treatment in experimental stroke.

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Lapergue, Bertrand; Dang, Bao Quoc; Desilles, Jean-Philippe; Ortiz-Munoz, Guadalupe; Delbosc, Sandrine; Loyau, Stéphane; Louedec, Liliane; Couraud, Pierre-Olivier; Mazighi, Mikael; Michel, Jean-Baptiste; Meilhac, Olivier; Amarenco, Pierre

2013-03-01

We have previously reported that intravenous injection of high-density lipoproteins (HDLs) was neuroprotective in an embolic stroke model. We hypothesized that HDL vasculoprotective actions on the blood-brain barrier (BBB) may decrease hemorrhagic transformation-associated with tissue plasminogen activator (tPA) administration in acute stroke. We used tPA alone or in combination with HDLs in vivo in 2 models of focal middle cerebral artery occlusion (MCAO) (embolic and 4-hour monofilament MCAO) and in vitro in a model of BBB. Sprague-Dawley rats were submitted to MCAO, n=12 per group. The rats were then randomly injected with tPA (10 mg/kg) or saline with or without human plasma purified-HDL (10 mg/kg). The therapeutic effects of HDL and BBB integrity were assessed blindly 24 hours later. The integrity of the BBB was also tested using an in vitro model of human cerebral endothelial cells under oxygen-glucose deprivation. tPA-treated groups had significantly higher mortality and rate of hemorrhagic transformation at 24 hours in both MCAO models. Cotreatment with HDL significantly reduced stroke-induced mortality versus tPA alone (by 42% in filament MCAO, P=0.009; by 73% in embolic MCAO, P=0.05) and tPA-induced intracerebral parenchymal hematoma (by 92% in filament MCAO, by 100% in embolic MCAO; Phemorrhagic transformation in rat models of MCAO. Both in vivo and in vitro results support the vasculoprotective action of HDLs on BBB under ischemic conditions.

Prodigiosin inhibits gp91{sup phox} and iNOS expression to protect mice against the oxidative/nitrosative brain injury induced by hypoxia-ischemia

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Chang, Chia-Che [Institute of Biomedical Sciences, National Chung-Hsing University, Taichung, Taiwan (China); Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan (China); Agricultural Biotechnology Center, National Chung-Hsing University, Taichung, Taiwan (China); Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan (China); Wang, Yea-Hwey [Department of Nursing, College of Medicine and Nursing, Hungkuang University, Taichung, Taiwan (China); Chern, Chang-Ming [Division of Neurovascular Disease, Neurological Institute, Taipei Veterans General Hospital and School of Medicine, National Yang-Ming University, Taipei, Taiwan (China); Liou, Kuo-Tong [Department of Chinese Martial Arts, Chinese Culture University, Taipei, Taiwan (China); Hou, Yu-Chang [Department of Chinese Medicine, Taoyuan General Hospital, Department of Health, Taiwan (China); Department of Nursing, Yuanpei University, Hsinchu, Taiwan (China); Department of Bioscience Technology, Chuan-Yuan Christian University, Taoyuan, Taiwan (China); Peng, Yu-Ta [Institute of Biomedical Sciences, National Chung-Hsing University, Taichung, Taiwan (China); Shen, Yuh-Chiang, E-mail: yuhcs@nricm.edu.tw [National Research Institute of Chinese Medicine, Taipei, Taiwan (China); Institute of Biomedical Sciences, National Chung-Hsing University, Taichung, Taiwan (China)

2011-11-15

This study aimed to explore the mechanisms by which prodigiosin protects against hypoxia-induced oxidative/nitrosative brain injury induced by middle cerebral artery occlusion/reperfusion (MCAo/r) injury in mice. Hypoxia in vitro was modeled using oxygen-glucose deprivation (OGD) followed by reoxygenation of BV-2 microglial cells. Our results showed that treatment of mice that have undergone MCAo/r injury with prodigiosin (10 and 100 {mu}g/kg, i.v.) at 1 h after hypoxia ameliorated MCAo/r-induced oxidative/nitrosative stress, brain infarction, and neurological deficits in the mice, and enhanced their survival rate. MCAo/r induced a remarkable production in the mouse brains of reactive oxygen species (ROS) and a significant increase in protein nitrosylation; this primarily resulted from enhanced expression of NADPH oxidase 2 (gp91{sup phox}), inducible nitric oxide synthase (iNOS), and the infiltration of CD11b leukocytes due to breakdown of blood-brain barrier (BBB) by activation of nuclear factor-kappa B (NF-{kappa}B). All these changes were significantly diminished by prodigiosin. In BV-2 cells, OGD induced ROS and nitric oxide production by up-regulating gp91{sup phox} and iNOS via activation of the NF-{kappa}B pathway, and these changes were suppressed by prodigiosin. In conclusion, our results indicate that prodigiosin reduces gp91{sup phox} and iNOS expression possibly by impairing NF-{kappa}B activation. This compromises the activation of microglial and/or inflammatory cells, which then, in turn, mediates prodigiosin's protective effect in the MCAo/r mice. -- Highlights: Black-Right-Pointing-Pointer Prodigiosin ameliorated brain infarction and deficits. Black-Right-Pointing-Pointer Prodigiosin protected against hypoxia/reperfusion-induced brain injury. Black-Right-Pointing-Pointer Prodigiosin diminished oxidative/nitrosativestress and leukocytes infiltration. Black-Right-Pointing-Pointer Prodigiosin reduced BBB breakdown. Black

Neuroprotection, learning and memory improvement of a standardized extract from Renshen Shouwu against neuronal injury and vascular dementia in rats with brain ischemia.

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Wan, Li; Cheng, Yufang; Luo, Zhanyuan; Guo, Haibiao; Zhao, Wenjing; Gu, Quanlin; Yang, Xu; Xu, Jiangping; Bei, Weijian; Guo, Jiao

2015-05-13

The Renshen Shouwu capsule (RSSW) is a patented Traditional Chinese Medicine (TCM), that has been proven to improve memory and is widely used in China to apoplexy syndrome and memory deficits. To investigate the neuroprotective and therapeutic effect of the Renshen Shouwu standardized extract (RSSW) on ischemic brain neuronal injury and impairment of learning and memory related to Vascular Dementia (VD) induced by a focal and global cerebral ischemia-reperfusion injury in rats. Using in vivo rat models of both focal ischemia/reperfusion (I/R) injuries induced by a middle cerebral artery occlusion (MCAO), and VD with transient global brain I/R neuronal injuries induced by a four-vessel occlusion (4-VO) in Sprague-Dawley (SD) rats, RSSW (50,100, and 200 mg kg(-1) body weights) and Egb761® (80 mg kg(-1)) were administered orally for 20 days (preventively 6 days+therapeutically 14 days) in 4-VO rats, and for 7 days (3 days preventively+4 days therapeutically) in MCAO rats. Learning and memory behavioral performance was assayed using a Morris water maze test including a place navigation trial and a spatial probe trial. Brain histochemical morphology and hippocampal neuron survival was quantified using microscope assay of a puffin brain/hippocampus slice with cresyl violet staining. MCAO ischemia/reperfusion caused infarct damage in rat brain tissue. 4-VO ischemia/reperfusion caused a hippocampal neuronal lesion and learning and memory deficits in rats. Administration of RSSW (50, 100, and 200mg/kg) or EGb761 significantly reduced the size of the insulted brain hemisphere lesion and improved the neurological behavior of MCAO rats. In addition, RSSW markedly reduced an increase in the brain infarct volume from an I/R-induced MCAO and reduced the cerebral water content in a dose-dependent way. Administration of RSSW also increased the pyramidal neuronal density in the hippocampus of surviving rats after transient global brain ischemia and improved the learning and memory

Delayed brain ischemia tolerance induced by electroacupuncture pretreatment is mediated via MCP-induced protein 1

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2013-01-01

Background Emerging studies have demonstrated that pretreatment with electroacupuncture (EA) induces significant tolerance to focal cerebral ischemia. The present study seeks to determine the involvement of monocyte chemotactic protein-induced protein 1 (MCPIP1), a recently identified novel modulator of inflammatory reactions, in the cerebral neuroprotection conferred by EA pretreatment in the animal model of focal cerebral ischemia and to elucidate the mechanisms of EA pretreatment-induced ischemic brain tolerance. Methods Twenty-four hours after the end of the last EA pretreatment, focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 90 minutes in male C57BL/6 mice and MCPIP1 knockout mice. Transcription and expression of MCPIP1 gene was monitored by qRT-PCR, Western blot and immunohistochemistry. The neurobehavioral scores, infarction volumes, proinflammatory cytokines and leukocyte infiltration in brain and NF-κB signaling were evaluated after ischemia/reperfusion. Results MCPIP1 protein and mRNA levels significantly increased specifically in mouse brain undergoing EA pretreatment. EA pretreatment significantly attenuated the infarct volume, neurological deficits, upregulation of proinflammatory cytokines and leukocyte infiltration in the brain of wild-type mice after MCAO compared with that of the non-EA group. MCPIP1-deficient mice failed to evoke EA pretreatment-induced tolerance compared with that of the control MCPIP1 knockout group without EA treatment. Furthermore, the activation of NF-κB signaling was significantly reduced in EA-pretreated wild-type mice after MCAO compared to that of the non-EA control group and MCPIP1-deficient mice failed to confer the EA pretreatment-induced inhibition of NF-κB signaling after MCAO. Conclusions Our data demonstrated that MCPIP1 deficiency caused significant lack of EA pretreatment-induced cerebral protective effects after MCAO compared with the control group and that MCPIP1 is

Protection and repair of post-thrombolytic brain tissue with high-dose human albumin and magnesium sulfate: an experimental study

International Nuclear Information System (INIS)

Li Yongdong; Zhao Jungong; Li Minghua; You Xiaofang; Chen Yingsheng

2008-01-01

Objective: To evaluate the neuroprotective effects of high-dose human albumin and magnesium sulfate combined with recombinant tissue plasminogen activator (rt-PA) thrombolysis in a SD rat model of embolic stroke, with the aim to explore the possibility of extention for thrombolytic window. Methods: A thromboembolic stroke model performed on male SD rats (n=40) was randomly assigned into four groups: group A (n=10): rats received an intravenous infusion of 10 mg/kg rt-PA over a period of one hour at 3 h after onset of MCAO; group B (n=10): rats received an intravenous infusion of 10 mg/kg rt-PA over a period of one hour at 6 h after onset of MCAO; group C(n=10): rats received an intravenous infusion of human albumin (2.5 g/kg) and rt-PA(10 mg/kg) at 3 h and 6 h after onset of MCAO; group D(n=10): rats received same dose human albumin and rt-PA as that in group C, in addition, magnesium salfate (500 mg/ kg) was given intraperitoneally 3 h and 18 h after onset of MCAO. MRI was performed in each animal at preischemia, 24 h, 7 d and 14 d after treatment. After the last MR examination, all animals were killed under anesthesia, pathologic study (including electron microscope, light microscope, immuno-histochemistry) was performed in each animal, and LSCM were performed in two animals of each group. Results: The infarct volumes in four groups at 14 d after thrombolysis reduced 5.07% , 2.58%, 10.18% and 35.40% respectively compared with the infarct volume at 3 h after MCAO, with a predominant reduction in group D (P<0.05); increase of rCBV was confirmed at the marginal area of the cerebral infarction from the onset of stroke to 14 d, with significant increase between group A and C from 1 d to 7 d (P<0.05), while no significant difference was found in group B and C. The longest survival exhibited in group D and the shortest in group B, and no significant difference occurred concerning about survival among the four groups (P=0.763, P=0.636). In addition, LSCM showed a slight

Neuroprotective capabilities of TSA against cerebral ischemia/reperfusion injury via PI3K/Akt signaling pathway in rats.

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Ma, Xiao-Hui; Gao, Qiang; Jia, Zhen; Zhang, Ze-Wei

2015-02-01

Hundreds of previous studies demonstrated the cytoprotective effect of trichostatin-A (TSA), a kind of histone deacetylases inhibitors (HDACIs), against cerebral ischemia/reperfusion insult. Meanwhile, phosphatidylinositol-3 kinase/Akt (PI3K/Akt) is a well-known, important signaling pathway that mediates neuroprotection. However, it should be remains unclear whether the neuroprotective capabilities of TSA against cerebral ischemia/reperfusion is mediated by activation of the PI3K/Akt signaling pathway. Five groups rats (n = 12 each), with middle cerebral artery occlusion (MCAO) except sham group, were used to investigate the neuroprotective effect of certain concentration (0.05 mg/kg) of TSA, and whether the neuroprotective effect of TSA is associated with activation of the PI3K/Akt signaling pathway through using of wortmannin (0.25 mg/kg). TSA significantly increased the expression of p-Akt protein, reduced infarct volume, and attenuated neurological deficit in rats with transient MCAO, wortmannin weakened such effect of TSA dramatically. TSA could significantly decrease the neurological deficit scores and reduce the cerebral infarct volume during cerebral ischemia/reperfusion injury, which was achieved partly by activation of the PI3K/Akt signaling pathway via upgrading of p-Akt protein.

Methotrexate carried in lipid core nanoparticles reduces myocardial infarction size and improves cardiac function in rats

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Maranhão RC

2017-05-01

Full Text Available Raul C Maranhão,1,2 Maria C Guido,1 Aline D de Lima,1 Elaine R Tavares,1 Alyne F Marques,1 Marcelo D Tavares de Melo,3 Jose C Nicolau,3 Vera MC Salemi,3 Roberto Kalil-Filho3 1Laboratory of Metabolism and Lipids, 2Faculty of Pharmaceutical Sciences, 3Heart Failure Unit, Clinical Cardiology Division, Heart Institute (InCor, Medical School Hospital, University of São Paulo, São Paulo, Brazil Purpose: Acute myocardial infarction (MI is accompanied by myocardial inflammation, fibrosis, and ventricular remodeling that, when excessive or not properly regulated, may lead to heart failure. Previously, lipid core nanoparticles (LDE used as carriers of the anti-inflammatory drug methotrexate (MTX produced an 80-fold increase in the cell uptake of MTX. LDE-MTX treatment reduced vessel inflammation and atheromatous lesions induced in rabbits by cholesterol feeding. The aim of the study was to investigate the effects of LDE-MTX on rats with MI, compared with commercial MTX treatment.Materials and methods: Thirty-eight Wistar rats underwent left coronary artery ligation and were treated with LDE-MTX, or with MTX (1 mg/kg intraperitoneally, once/week, starting 24 hours after surgery or with LDE without drug (MI-controls. A sham-surgery group (n=12 was also included. Echocardiography was performed 24 hours and 6 weeks after surgery. The animals were euthanized and their hearts were analyzed for morphometry, protein expression, and confocal microscopy.Results: LDE-MTX treatment achieved a 40% improvement in left ventricular (LV systolic function and reduced cardiac dilation and LV mass, as shown by echocardiography. LDE-MTX reduced the infarction size, myocyte hypertrophy and necrosis, number of inflammatory cells, and myocardial fibrosis, as shown by morphometric analysis. LDE-MTX increased antioxidant enzymes; decreased apoptosis, macrophages, reactive oxygen species production; and tissue hypoxia in non-infarcted myocardium. LDE-MTX increased adenosine

The broad-spectrum cation channel blocker pinokalant (LOE 908 MS) reduces brain infarct volume in rats

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Christensen, Thomas; Wienrich, Marion; Ensinger, Helmut A

2005-01-01

this period and the spontaneous temperature after course in control rats established in other experiments was imitated. Seven days later histological brain sections were prepared and the infarct volumes measured. Body temperature did not differ between the groups. Mean arterial blood pressure was slightly...... higher in the pinokalant group. Pinokalant treatment significantly reduced cortical infarct volume from 33.8+/-15.8 mm3 to 24.5+/-13.1 mm3 (control group versus pinokalant group, P=0.017, t-test). Taking the effective drug plasma concentration established in other experiments into account revealed...... and electrophysiologic status of the ischemic penumbra and to reduce lesion size on magnetic resonance images in the acute phase following middle cerebral artery occlusion in rats. The purpose of the present study was to investigate whether these beneficial effects of pinokalant are translated into permanent...

Protective Effects of Dihydrocaffeic Acid, a Coffee Component Metabolite, on a Focal Cerebral Ischemia Rat Model

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Kyungjin Lee

2015-06-01

Full Text Available We recently reported the protective effects of chlorogenic acid (CGA in a transient middle cerebral artery occlusion (tMCAo rat model. The current study further investigated the protective effects of the metabolites of CGA and dihydrocaffeic acid (DHCA was selected for further study after screening using the same tMCAo rat model. In the current study, tMCAo rats (2 h of MCAo followed by 22 h of reperfusion were injected with various doses of DHCA at 0 and 2 h after onset of ischemia. We assessed brain damage, functional deficits, brain edema, and blood-brain barrier damage at 24 h after ischemia. For investigating the mechanism, in vitro zymography and western blotting analysis were performed to determine the expression and activation of matrix metalloproteinase (MMP-2 and -9. DHCA (3, 10, and 30 mg/kg, i.p. dose-dependently reduced brain infarct volume, behavioral deficits, brain water content, and Evans Blue (EB leakage. DHCA inhibited expression and activation of MMP-2 and MMP-9. Therefore, DHCA might be one of the important metabolites of CGA and of natural products, including coffee, with protective effects on ischemia-induced neuronal damage and brain edema.

Treatment with the C5a receptor antagonist ADC-1004 reduces myocardial infarction in a porcine ischemia-reperfusion model

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Arheden Håkan

2010-09-01

Full Text Available Abstract Background Polymorphonuclear neutrophils, stimulated by the activated complement factor C5a, have been implicated in cardiac ischemia/reperfusion injury. ADC-1004 is a competitive C5a receptor antagonist that has been shown to inhibit complement related neutrophil activation. ADC-1004 shields the neutrophils from C5a activation before they enter the reperfused area, which could be a mechanistic advantage compared to previous C5a directed reperfusion therapies. We investigated if treatment with ADC-1004, according to a clinically applicable protocol, would reduce infarct size and microvascular obstruction in a large animal myocardial infarct model. Methods In anesthetized pigs (42-53 kg, a percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 minutes, followed by 4 hours of reperfusion. Twenty minutes after balloon inflation the pigs were randomized to an intravenous bolus administration of ADC-1004 (175 mg, n = 8 or saline (9 mg/ml, n = 8. Area at risk (AAR was evaluated by ex vivo SPECT. Infarct size and microvascular obstruction were evaluated by ex vivo MRI. The observers were blinded to the treatment at randomization and analysis. Results ADC-1004 treatment reduced infarct size by 21% (ADC-1004: 58.3 ± 3.4 vs control: 74.1 ± 2.9%AAR, p = 0.007. Microvascular obstruction was similar between the groups (ADC-1004: 2.2 ± 1.2 vs control: 5.3 ± 2.5%AAR, p = 0.23. The mean plasma concentration of ADC-1004 was 83 ± 8 nM at sacrifice. There were no significant differences between the groups with respect to heart rate, mean arterial pressure, cardiac output and blood-gas data. Conclusions ADC-1004 treatment reduces myocardial ischemia-reperfusion injury and represents a novel treatment strategy of myocardial infarct with potential clinical applicability.

The sensorimotor and cognitive deficits in rats following 90- and 120-min transient occlusion of the middle cerebral artery.

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Zvejniece, Liga; Svalbe, Baiba; Liepinsh, Edgars; Pulks, Eduards; Dambrova, Maija

2012-07-15

Middle cerebral artery occlusion (MCAO) is the most commonly used method to study the neurological and histological outcomes and the pathological mechanisms of ischaemic stroke. The current work compares sensorimotor and cognitive deficits and the infarct volume in rats following a transient 90- or 120-min MCAO, which allows the appropriate behavioural tests to be chosen based on the goal and design of the experiment. In the beam-walking test, we found significant differences between the 90- and 120-min MCAO groups in the number of foot faults made with the impaired hindlimb on post-stroke days 3, 7 and 14. In the cylinder test, a difference between the 90- and 120-min groups was observed on post-operation day 14. The responses to tactile and proprioceptive stimulation were impaired to a similar extent after 90- and 120-min MCAO in the vibrissae-evoked forelimb-placing and limb-placing tests. Moreover, we found significant memory impairment in the 120-min MCAO group 6 days after the acquisition trial. The brain tissue damage was significantly higher after 120-min occlusion of the MCA compared with 90-min occlusion; the infarct volumes were 13% and 25% of the contralateral hemispheres, respectively. In conclusion, both the 90- and 120-min occlusion models result in a significant impairment of sensorimotor, tactile and proprioceptive function, but memory impairment is only observed in the 120-min MCAO group. The beam-walking and cylinder tests detected neurological dysfunction after the 120-min MCAO, whereas the limb-placing and vibrissae-evoked forelimb-placing tests were able to evaluate the neurological dysfunction in rats after 90- and 120-min MCAO. Copyright © 2012 Elsevier B.V. All rights reserved.

Non-Q-wave myocardial infarction: impaired myocardial energy metabolism in regions with reduced 99mTc-MIBI accumulation.

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Moka, D; Baer, F M; Theissen, P; Schneider, C A; Dietlein, M; Erdmann, E; Schicha, H

2001-05-01

Reduced regional technetium-99m methoxyisobutylisonitrile (99mTc-MIBI) accumulation in patients with chronic non-Q-wave infarction (NQWI) but without significant coronary artery stenosis indicates non-transmural damage of the myocardial wall. The aim of this study was to characterise cardiac energy metabolism after NQWI using phosphorus-31 magnetic resonance spectroscopy (31P-MRS) and to compare the biochemical remodelling with changes in regional 99mTc-MIBI uptake and with morphological and functional parameters assessed by magnetic resonance imaging (MRI). Fifteen patients with a history of NQWI, exclusion of significant coronary artery stenosis (energy metabolism. Spectroscopic measurements were performed in the infarct-related myocardial region. Corresponding gradient-echo MR images and myocardial 99mTc-MIBI single-photon emission tomography images were acquired for exact localisation of the infarct region. All examinations were performed at rest under anti-ischaemic medication. Data were compared with those of patients in whom coronary artery disease had been excluded by angiography (group B, n=10). All patients of group A displayed anterior wall hypokinesia in the infarcted area on both ventriculography and MRI, with a reduced myocardial accumulation of 99mTc-MIBI (66.3%+/-11.8% vs 95.6%+/-2.2% in group B). The mean wall thickness during the complete cardiac cycle (9.5+/-1.8 mm vs 13.1+/-1.1 mm in group B, Penergy metabolism.

Angiotensin AT2-receptor stimulation improves survival and neurological outcome after experimental stroke in mice

DEFF Research Database (Denmark)

Schwengel, Katja; Namsolleck, Pawel; Lucht, Kristin

2016-01-01

/BL6J or AT2R-knockout mice (AT2-KO) underwent MCAO for 30 min followed by reperfusion. Starting 45 min after MCAO, mice were treated once daily for 4 days with either vehicle or C21 (0.03 mg/kg ip). Neurological deficits were scored daily. Infarct volumes were measured 96 h post-stroke by MRI. C21...

Increased myocardial infarct size because of reduced coronary collateral blood flow in beagles

International Nuclear Information System (INIS)

Uemura, N.; Knight, D.R.; Shen, Y.T.; Nejima, J.; Cohen, M.V.; Thomas, J.X. Jr.; Vatner, S.F.

1989-01-01

Effects of permanent left circumflex coronary artery occlusion (CAO) were examined in conscious purebred beagles and mongrel dogs, instrumented with miniature left ventricular (LV) pressure gauges, wall thickness gauges in the ischemic zone, catheters in left atrium and aorta, and snares around the left circumflex coronary artery. Blood flow was measured using the radioactive microsphere technique before CAO and at 5 min, 1, 3, and 24 h after CAO. Although CAO reduced myocardial blood flow similarly in beagles and mongrels, significantly less (P less than 0.05) recovery of myocardial blood flow was observed over the following 24-h period in beagles. Infarct size, as determined by triphenyltetrazolium chloride and expressed as percentage of area at risk, was larger (P less than 0.05) in beagles (62.0 ± 5.1%) than mongrels (42.5 ± 4.2%). Thus beagles do not tolerate ischemia as well as mongrel dogs and possess fewer functional coronary collaterals resulting in larger infarcts after CAO

Prolonged drug-induced hypothermia in experimental stroke

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Johansen, Flemming Fryd; Jørgensen, Henrik Stig; Reith, Jakob

2007-01-01

In experimental and human stroke, hypothermia is strongly related to a favorable outcome. Previous attempts to manipulate the core temperature in focal cerebral ischemia have been based on mechanical cooling. The purpose of the study is to establish a model for long-term drug-induced hypothermia...... in focal ischemia by pharmacological alteration of the central thermoregulatory set-point. We tested the hypothesis that the dopaminergic agonist Talipexole, which induces hypothermia, reduces infarct size. Body temperature was monitored by a radio-pill-implant. Rats had reversible occlusion of the middle...... that the core body temperature was reduced by 1.7 degrees C for 24 hours after MCAO in rats treated with Talipexole. This treatment induced a significant reduction of infarct volume at 7 days after focal ischemia by 47%. We suggest that the reduction in infarct volume is related to drug-induced hypothermia...

Purinergic receptor stimulation reduces cytotoxic edema and brain infarcts in mouse induced by photothrombosis by energizing glial mitochondria.

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Wei Zheng

2010-12-01

Full Text Available Treatments to improve the neurological outcome of edema and cerebral ischemic stroke are severely limited. Here, we present the first in vivo single cell images of cortical mouse astrocytes documenting the impact of single vessel photothrombosis on cytotoxic edema and cerebral infarcts. The volume of astrocytes expressing green fluorescent protein (GFP increased by over 600% within 3 hours of ischemia. The subsequent growth of cerebral infarcts was easily followed as the loss of GFP fluorescence as astrocytes lysed. Cytotoxic edema and the magnitude of ischemic lesions were significantly reduced by treatment with the purinergic ligand 2-methylthioladenosine 5' diphosphate (2-MeSADP, an agonist with high specificity for the purinergic receptor type 1 isoform (P2Y(1R. At 24 hours, cytotoxic edema in astrocytes was still apparent at the penumbra and preceded the cell lysis that defined the infarct. Delayed 2MeSADP treatment, 24 hours after the initial thrombosis, also significantly reduced cytotoxic edema and the continued growth of the brain infarction. Pharmacological and genetic evidence are presented indicating that 2MeSADP protection is mediated by enhanced astrocyte mitochondrial metabolism via increased inositol trisphosphate (IP(3-dependent Ca(2+ release. We suggest that mitochondria play a critical role in astrocyte energy metabolism in the penumbra of ischemic lesions, where low ATP levels are widely accepted to be responsible for cytotoxic edema. Enhancement of this energy source could have similar protective benefits for a wide range of brain injuries.

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage

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Jian-Min Piao

2018-04-01

Full Text Available Background/Aims: Acute cerebral ischemia is a manifestation of cerebral vascular insufficiency and has a high mortality. However, the therapy for acute cerebral ischemia is still limited. This study aimed to investigate the effect of microRNA-381 (miR-381 on the repair of nerve injury in rats with acute cerebral ischemia after cerebral lymphatic blockage (CLB by targeting leucine-rich repeat C4 protein (LRRC4 through the Stromal cell-derived factor-1/CXC chemokine receptor-4 signaling pathway. Methods: Rat models of CLB and middle cerebral artery occlusion (MCAO were established, and 56 Wistar rats were divided into sham, MCAO, CLB + MCAO, CLB + MCAO + miR-381 inhibitor, CLB + MCAO + miR-381 mimic, CLB + MCAO + AMD3100 and CLB + MCAO + miR-381 mimic + AMD3100 groups. Modified neurological severity score (mNSS was used to determine nerve injury, TTC staining to measure infarction volume, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL staining and flow cytometry to evaluate cell apoptosis, immunofluorescence to measure BrdU-positive cell number, enzyme-linked immunosorbent assay (ELISA to determine contents of tumor necrosis factor-α (TNF-α, interleukin-1β (IL-1β, interleukin-6 (IL-6, interleukin-10 (IL-10, nerve growth factor (NGF and neurite outgrowth inhibitor -A (Nogo-A, Reverse transcription quantitative polymerase chain reaction (RT-qPCR and Western blotting to evaluate expression of miR-381, LRRC4, SDF-1, CXCR4, pERK, Slit2 and vascular endothelial growth factor (VEGF. Results: LRRC4 was a target gene of miR-381. Compared with the results in the CLB + MCAO group, mNSS, infarction volume, apoptosis rate and TNF-α, IL-1β, IL-6 and Nogo-A contents as well as LRRC4 expression in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups were increased (those in the CLB + MCAO + AMD3100 group > those in the CLB + MCAO + miR-381 mimic + AMD3100 group, while BrdU-positive cell number, contents of NGF and

Effects of acupuncture at GV20 and ST36 on the expression of matrix metalloproteinase 2, aquaporin 4, and aquaporin 9 in rats subjected to cerebral ischemia/reperfusion injury.

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Hong Xu

Full Text Available BACKGROUND/PURPOSE: Ischemic stroke is characterized by high morbidity and mortality worldwide. Matrix metalloproteinase 2 (MMP2, aquaporin (AQP 4, and AQP9 are linked to permeabilization of the blood-brain barrier (BBB in cerebral ischemia/reperfusion injury (CIRI. BBB disruption, tissue inflammation, and MMP/AQP upregulation jointly provoke brain edema/swelling after CIRI, while acupuncture and electroacupuncture can alleviate CIRI symptoms. This study evaluated the hypothesis that acupuncture and electroacupuncture can similarly exert neuroprotective actions in a rat model of middle cerebral artery occlusion (MCAO by modulating MMP2/AQP4/APQ9 expression and inflammatory cell infiltration. METHODS: Eighty 8-week-old Sprague-Dawley rats were randomly divided into sham group S, MCAO model group M, acupuncture group A, electroacupuncture group EA, and edaravone group ED. The MCAO model was established by placement of a suture to block the middle carotid artery, and reperfusion was triggered by suture removal in all groups except group S. Acupuncture and electroacupuncture were administered at acupoints GV20 (governing vessel-20 and ST36 (stomach-36. Rats in groups A, EA, and ED received acupuncture, electroacupuncture, or edaravone, respectively, immediately after MCAO. Neurological function (assessed using the Modified Neurological Severity Score, infarct volume, MMP2/AQP4/AQP9 mRNA and protein expression, and inflammatory cell infiltration were all evaluated at 24 h post-reperfusion. RESULTS: Acupuncture and electroacupuncture significantly decreased infarct size and improved neurological function. Furthermore, target mRNA and protein levels and inflammatory cell infiltration were significantly reduced in groups A, EA, and ED vs. group M. However, MMP2/AQP levels and inflammatory cell infiltration were generally higher in groups A and EA than in group ED except MMP2 mRNA levels. CONCLUSIONS: Acupuncture and electroacupuncture at GV20 and ST36

PR-957 mediates neuroprotection by inhibiting Th17 differentiation and modulating cytokine production in a mouse model of ischaemic stroke.

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Guo, Y; Chen, X; Li, D; Liu, H; Ding, Y; Han, R; Shi, Y; Ma, X

2018-03-30

Acute ischaemic stroke can induce secondary brain injury by activating an inflammatory response that contributes to clinical impairment. As a specific inhibitor of the immunoproteasome subunit low molecular weight polypeptide 7 (LMP7), PR-957 may participate in regulating pathophysiological and inflammatory responses in multiple diseases of the central nervous system (CNS). We investigated the neuroprotective properties of PR-957 in a mouse model of stroke, induced by middle cerebral artery occlusion (MCAO). After MCAO and injections of PR-957 or vehicle, we evaluated mice behaviourally using modified Neurological Severity Scores (mNSS) and sensorimotor tests, including the adhesive-removal test, a foot-fault test and an inclined plane test. Infarct volume was measured 24 and 72 h after MCAO. Infiltration by different lymphocyte subpopulations was evaluated by flow cytometry and immunofluorescent staining of brain tissue from the penumbral area. Quantitative real-time polymerase chain reaction analysis and enzyme-linked immunosorbent assay were used to measure the expression of proinflammatory cytokines: interkeukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IL-17A, interferon (IFN)-γ, tumour necrosis factor (TNF)-α, granulocyte colony-stimulating factor (GCSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF). Expression of phosphorylated signal transducer and activator of transcription 3 (pSTAT-3) protein levels in brain was measured by immunoblot. MCAO mice treated with PR-957 showed a significant decrease in infarct volume and had mild neurological deficits compared to vehicle-treated mice. PR-957 administration also significantly decreased IL-1β, IL-6, IL-12, IL-17A and TNF-α. PR-957 provides neuroprotection via inhibiting T lymphocyte infiltration and decreasing T helper type 17 (Th17) cell differentiation in MCAO mice, which may result from the reduced expression of pSTAT-3. The neuroprotective effect of PR-957 indicates its

By Improving Regional Cortical Blood Flow, Attenuating Mitochondrial Dysfunction and Sequential Apoptosis Galangin Acts as a Potential Neuroprotective Agent after Acute Ischemic Stroke

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Ming Cheng

2012-11-01

Full Text Available Ischemic stroke is a devastating disease with a complex pathophysiology. Galangin is a natural flavonoid isolated from the rhizome of Alpina officinarum Hance, which has been widely used as an antioxidant agent. However, its effects against ischemic stroke have not been reported and its related neuroprotective mechanism has not really been explored. In this study, neurological behavior, cerebral infarct volumes and the improvement of the regional cortical blood flow (rCBF were used to evaluate the therapeutic effect of galangin in rats impaired by middle cerebral artery occlusion (MCAO-induced focal cerebral ischemia. Furthermore, the determination of mitochondrial function and Western blot of apoptosis-related proteins were performed to interpret the neuroprotective mechanism of galangin. The results showed that galangin alleviated the neurologic impairments, reduced cerebral infarct at 24 h after MCAO and exerted a protective effect on the mitochondria with decreased production of mitochondrial reactive oxygen species (ROS. These effects were consistent with improvements in the membrane potential level (Dym, membrane fluidity, and degree of mitochondrial swelling in a dose-dependent manner. Moreover, galangin significantly improved the reduced rCBF after MCAO. Western blot analysis revealed that galangin also inhibited apoptosis in a dose-dependent manner concomitant with the up-regulation of Bcl-2 expression, down-regulation of Bax expression and the Bax/Bcl-2 ratio, a reduction in cytochrome c release from the mitochondria to the cytosol, the reduced expression of activated caspase-3 and the cleavage of poly(ADP-ribose polymerase (PARP. All these data in this study demonstrated that galangin might have therapeutic potential for ischemic stroke and play its protective role through the improvement in rCBF, mitochondrial protection and inhibiting caspase-dependent mitochondrial cell death pathway for the first time.

By improving regional cortical blood flow, attenuating mitochondrial dysfunction and sequential apoptosis galangin acts as a potential neuroprotective agent after acute ischemic stroke.

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Li, Shaojing; Wu, Chuanhong; Zhu, Li; Gao, Jian; Fang, Jing; Li, Defeng; Fu, Meihong; Liang, Rixin; Wang, Lan; Cheng, Ming; Yang, Hongjun

2012-11-09

Ischemic stroke is a devastating disease with a complex pathophysiology. Galangin is a natural flavonoid isolated from the rhizome of Alpina officinarum Hance, which has been widely used as an antioxidant agent. However, its effects against ischemic stroke have not been reported and its related neuroprotective mechanism has not really been explored. In this study, neurological behavior, cerebral infarct volumes and the improvement of the regional cortical blood flow (rCBF) were used to evaluate the therapeutic effect of galangin in rats impaired by middle cerebral artery occlusion (MCAO)-induced focal cerebral ischemia. Furthermore, the determination of mitochondrial function and Western blot of apoptosis-related proteins were performed to interpret the neuroprotective mechanism of galangin. The results showed that galangin alleviated the neurologic impairments, reduced cerebral infarct at 24 h after MCAO and exerted a protective effect on the mitochondria with decreased production of mitochondrial reactive oxygen species (ROS). These effects were consistent with improvements in the membrane potential level (Dym), membrane fluidity, and degree of mitochondrial swelling in a dose-dependent manner. Moreover, galangin significantly improved the reduced rCBF after MCAO. Western blot analysis revealed that galangin also inhibited apoptosis in a dose-dependent manner concomitant with the up-regulation of Bcl-2 expression, down-regulation of Bax expression and the Bax/Bcl-2 ratio, a reduction in cytochrome c release from the mitochondria to the cytosol, the reduced expression of activated caspase-3 and the cleavage of poly(ADP-ribose) polymerase (PARP). All these data in this study demonstrated that galangin might have therapeutic potential for ischemic stroke and play its protective role through the improvement in rCBF, mitochondrial protection and inhibiting caspase-dependent mitochondrial cell death pathway for the first time.

Mozart, but not the Beatles, reduces systolic blood pressure in patients with myocardial infarction.

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Gruhlke, Luiza Carolina; Patrício, Marcelo Coelho; Moreira, Daniel Medeiros

2015-12-01

Music reduces systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) in various clinical situations, but it is unclear whether these changes occur in post-infarction patients. The aim is to evaluate the effects of music on patients with acute myocardial infarction (MI). We evaluated patients with MI and we measured SBP, DBP, HR and double product (DP) two times before the intervention and one time every fifteen minutes with an ambulatory blood pressure monitor. We divided the patients into 3 groups: a group listening to music by Mozart; another listening to a Beatles collection and a third one listening to the radio news. Outcomes were the change in mean SBP, DBP, HR and DP with intervention. We enrolled 60 patients (20 in each group). SBP was significantly reduced in the Mozart group (variation of –7.2 ± 8.5 mmHg) compared to the Beatles group (–1.3 ± 6.2 mmHg) (P = 0.021) and the radio news group (0.6 ± 8.7 mmHg) (P = 0.003). DP was significantly reduced in the Mozart group compared with the News group (–668.5 ± 773.2 vs 31.6 ± 722.1 mmHg) (P = 0.006). There were no differences in DBP and HR. Patients with MI who listened Mozart had a reduction in SBP and DP compared to those who listened to the Beatles or the news.

Preconditioning with the traditional Chinese medicine Huang-Lian-Jie-Du-Tang initiates HIF-1α-dependent neuroprotection against cerebral ischemia in rats.

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Zhang, Qichun; Bian, Huimin; Li, Yu; Guo, Liwei; Tang, Yuping; Zhu, Huaxu

2014-06-11

Huang-Lian-Jie-Du-Tang (HLJDT) is a classical heat-clearing and detoxicating formula of traditional Chinese medicine that is widely used to treat stroke. The present study was designed to investigate the effects of HLJDT preconditioning on neurons under oxygen and glucose deprivation (OGD) and rats subjected to middle cerebral artery occlusion (MCAO). A stroke model of rats was obtained through MCAO. Following HLJDT preconditioning, the cerebral infarction volume, cerebral water content, and neurological deficient score were determined. Cerebral cortical neurons cultured in vitro were preconditioned with HLJDT and then subjected to OGD treatment. The release of lactate dehydrogenase (LDH) from neurons was detected. The levels of hypoxia-inducible factor-1α (HIF-1α) and PI3K/Akt signaling were analyzed by western blotting, and the levels of erythropoietin (EPO) and vascular endothelial growth factor (VEGF) in the supernatant of the neurons and the plasma of MCAO rats were measured through a radioimmunological assay. The apoptosis and proliferation of neurons were analyzed by immunohistochemistry. HLJDT preconditioning significantly reduced the cerebral infarction volume and cerebral water content and ameliorated the neurological deficient score of MCAO rats. In addition, HLJDT preconditioning protected neurons against OGD. Increased HIF-1α, EPO, and VEGF levels and the activation of PI3K/Akt signaling were observed as a result of HLJDT preconditioning. Furthermore, HLJDT preconditioning was found to inhibit ischemia-induced neuron apoptosis and to promote neuron proliferation under conditions of ischemia/reperfusion. Both rats and neurons subjected to HLJDT preconditioning were able to resist ischemia/reperfusion or hypoxia injury through the inhibition of apoptosis and the enhancement of proliferation, and these effects were primarily dependent on the activation of the PI3K/Akt signaling pathway and HIF-1α. Copyright © 2014 Elsevier Ireland Ltd. All rights

Dietary red palm oil supplementation reduces myocardial infarct size in an isolated perfused rat heart model

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Esterhuyse Adriaan J

2010-06-01

Full Text Available Abstract Background and Aims Recent studies have shown that dietary red palm oil (RPO supplementation improves functional recovery following ischaemia/reperfusion in isolated hearts. The main aim of this study was to investigate the effects of dietary RPO supplementation on myocardial infarct size after ischaemia/reperfusion injury. The effects of dietary RPO supplementation on matrix metalloproteinase-2 (MMP2 activation and PKB/Akt phosphorylation were also investigated. Materials and methods Male Wistar rats were divided into three groups and fed a standard rat chow diet (SRC, a SRC supplemented with RPO, or a SRC supplemented with sunflower oil (SFO, for a five week period, respectively. After the feeding period, hearts were excised and perfused on a Langendorff perfusion apparatus. Hearts were subjected to thirty minutes of normothermic global ischaemia and two hours of reperfusion. Infarct size was determined by triphenyltetrazolium chloride staining. Coronary effluent was collected for the first ten minutes of reperfusion in order to measure MMP2 activity by gelatin zymography. Results Dietary RPO-supplementation decreased myocardial infarct size significantly when compared to the SRC-group and the SFO-supplemented group (9.1 ± 1.0% versus 30.2 ± 3.9% and 27.1 ± 2.4% respectively. Both dietary RPO- and SFO-supplementation were able to decrease MMP2 activity when compared to the SRC fed group. PKB/Akt phosphorylation (Thr 308 was found to be significantly higher in the dietary RPO supplemented group when compared to the SFO supplemented group at 10 minutes into reperfusion. There was, however, no significant changes observed in ERK phosphorylation. Conclusions Dietary RPO-supplementation was found to be more effective than SFO-supplementation in reducing myocardial infarct size after ischaemia/reperfusion injury. Both dietary RPO and SFO were able to reduce MMP2 activity, which suggests that MMP2 activity does not play a major role in

Ischemic lesion volume determination on diffusion weighted images vs. apparent diffusion coefficient maps.

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Bråtane, Bernt Tore; Bastan, Birgul; Fisher, Marc; Bouley, James; Henninger, Nils

2009-07-07

Though diffusion weighted imaging (DWI) is frequently used for identifying the ischemic lesion in focal cerebral ischemia, the understanding of spatiotemporal evolution patterns observed with different analysis methods remains imprecise. DWI and calculated apparent diffusion coefficient (ADC) maps were serially obtained in rat stroke models (MCAO): permanent, 90 min, and 180 min temporary MCAO. Lesion volumes were analyzed in a blinded and randomized manner by 2 investigators using (i) a previously validated ADC threshold, (ii) visual determination of hypointense regions on ADC maps, and (iii) visual determination of hyperintense regions on DWI. Lesion volumes were correlated with 24 hour 2,3,5-triphenyltetrazoliumchloride (TTC)-derived infarct volumes. TTC-derived infarct volumes were not significantly different from the ADC and DWI-derived lesion volumes at the last imaging time points except for significantly smaller DWI lesions in the pMCAO model (p=0.02). Volumetric calculation based on TTC-derived infarct also correlated significantly stronger to volumetric calculation based on last imaging time point derived lesions on ADC maps than DWI (pdetermined lesion volumes on ADC maps and DWI by both investigators correlated significantly with threshold-derived lesion volumes on ADC maps with the former method demonstrating a stronger correlation. There was also a better interrater agreement for ADC map analysis than for DWI analysis. Ischemic lesion determination by ADC was more accurate in final infarct prediction, rater independent, and provided exclusive information on ischemic lesion reversibility.

Twenty-four hours hypothermia has temporary efficacy in reducing brain infarction and inflammation in aged rats

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Sandu, Raluca Elena; Buga, Ana Maria; Balseanu, Adrian Tudor

2016-01-01

in aged animals. Because the duration of hypothermia in most clinical trials is between 24 and 48 hours, we questioned whether 24 hours exposure to gaseous hypothermia confers the same neuroprotective efficacy as 48 hours exposure. We found that a shorter exposure to hypothermia transiently reduced both...... inflammation and infarct size. However, after 1 week, the infarct size became even larger than in controls and after 2 weeks there was no beneficial effect on regenerative processes such as neurogenesis. Behaviorally, hypothermia also had a limited beneficial effect. Finally, after hydrogen sulfide......-induced hypothermia, the poststroke aged rats experienced a persistent sleep impairment during their active nocturnal period. Our data suggest that cellular events that are delayed by hypothermia in aged rats may, in the long term, rebound, and diminish the beneficial effects....

Intermittent fasting attenuates increases in neurogenesis after ischemia and reperfusion and improves recovery.

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Manzanero, Silvia; Erion, Joanna R; Santro, Tomislav; Steyn, Frederik J; Chen, Chen; Arumugam, Thiruma V; Stranahan, Alexis M

2014-05-01

Intermittent fasting (IF) is neuroprotective across a range of insults, but the question of whether extending the interval between meals alters neurogenesis after ischemia remains unexplored. We therefore measured cell proliferation, cell death, and neurogenesis after transient middle cerebral artery occlusion (MCAO) or sham surgery (SHAM) in mice fed ad libitum (AL) or maintained on IF for 3 months. IF was associated with twofold reductions in circulating levels of the adipocyte cytokine leptin in intact mice, but also prevented further reductions in leptin after MCAO. IF/MCAO mice also exhibit infarct volumes that were less than half those of AL/MCAO mice. We observed a 30% increase in basal cell proliferation in the hippocampus and subventricular zone (SVZ) in IF/SHAM, relative to AL/SHAM mice. However, cell proliferation after MCAO was limited in IF mice, which showed twofold increases in cell proliferation relative to IF/SHAM, whereas AL/MCAO mice exhibit fivefold increases relative to AL/SHAM. Attenuation of stroke-induced neurogenesis was correlated with reductions in cell death, with AL/MCAO mice exhibiting twice the number of dying cells relative to IF/MCAO mice. These observations indicate that IF protects against neurological damage in ischemic stroke, with circulating leptin as one possible mediator.

Anti-ischemic effect of curcumin in rat brain.

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Shukla, Pradeep K; Khanna, Vinay K; Ali, Mohd M; Khan, Mohd Y; Srimal, Rikhab C

2008-06-01

Turmeric has been in use since ancient times as a condiment and due to its medicinal properties. Curcumin, the yellow colouring principle in turmeric, is polyphenolic and major active constituent. Besides anti-inflammatory, thrombolytic and anticarcinogenic activities, curcumin also possesses strong antioxidant property. In view of the novel combination of properties, neuroprotective efficacy of curcumin was studied in rat middle cerebral artery occlusion (MCAO) model. Rats were subjected to 2 h of focal ischemia followed by 72 h of reperfusion. They were pre-treated with curcumin (100 mg/kg, po) for 5 days prior to MCAO and for another 3 days after MCAO. The parameters studied were behavioural, biochemical and histological. Treatment with curcumin could significantly improve neurobehavioral performance compared to untreated ischemic rats as judged by its effect on rota-rod performance and grid walking. A significant inhibition in lipid peroxidation and an increase in superoxide dismutase (SOD) activity in corpus striatum and cerebral cortex was observed following treatment with curcumin in MCAO rats as compared to MCAO group. Intracellular calcium levels were decreased following treatment with curcumin in MCAO rats. Histologically, a reduction in the infarct area from 33% to 24% was observed in MCAO rats treated with curcumin. The study demonstrates the protective efficacy of curcumin in rat MCAO model.

Targeted Temperature Management at 33°C or 36°C Produces Equivalent Neuroprotective Effects in the Middle Cerebral Artery Occlusion Rat Model of Ischemic Stroke.

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Lee, Jung Ho; Lim, Jisoo; Chung, Yong Eun; Chung, Sung Phil; Park, Incheol; Kim, Chul Hoon; You, Je Sung

2018-01-15

Targeted temperature management (TTM, 32°C to 36°C) is one of the most successful achievements in modern resuscitation medicine. It has become standard treatment for survivors of sudden cardiac arrest to minimize secondary brain damage. TTM at 36°C is just as effective as TTM at 33°C and is actually preferred because it reduces adverse TTM-associated effects. TTM also likely has direct neuroprotective effects in ischemic brains in danger of stroke. It remains unclear, however, whether higher temperature TTM is equally effective in protecting the brain from the effects of stroke. Here, we asked whether TTM at 36°C is as effective as TTM at 33°C in improving outcomes in a middle cerebral artery occlusion (MCAO) model of ischemic stroke. After dividing rats randomly into MCAO, MCAO+33°C TTM, MCAO+36°C TTM and sham groups, we subjected all of them except for the sham group to MCAO for 3 h (for the behavioral tests) or 4 h (for all other biochemical analyses). We found TTM protocols at both 33°C and 36°C produce comparable reductions of infarct volumes in the MCAO territory and equally attenuate the extracellular release of high mobility group box 1 (HMGB1) in post-ischemic brains. Both TTM conditions prevent the mRNA induction of a major pro-inflammatory cytokine, TNF-α, in the ischemic penumbra region. Finally, both TTM protocols produce similar improvements in neurological outcomes in rats, as measured by a battery of behavior tests 21 h after the start of reperfusion. These data acquired in a rat MCAO model suggest TTM at 36°C has excellent therapeutic potential for improving clinical outcomes for patients with acute ischemic stroke.

In vivo MRI assessment of permanent middle cerebral artery occlusion by electrocoagulation: pitfalls of procedure

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2010-01-01

Permanent middle cerebral artery (MCA) occlusion (pMCAO) by electrocoagulation is a commonly used model but with potential traumatic lesions. Early MRI monitoring may assess pMCAO for non-specific brain damage. The surgical steps of pMCAO were evaluated for traumatic cerebral injury in 22 Swiss mice using diffusion and T2-weighted MRI (7T) performed within 1 h and 24 h after surgery. Temporal muscle cauterization without MCA occlusion produced an early T2 hyperintensity mimicking an infarct. No lesion was visible after temporal muscle incision or craniotomy. Early MRI monitoring is useful to identify non-specific brain injury that could hamper neuroprotective drugs assessment. PMID:20298536

褐藻多糖硫酸酯对大鼠脑缺血再灌注损伤后的神经保护作用%Neuroprotective Effect of Fucoidan in Rats after Cerebral Ischemia-reperfusion Injury

Institute of Scientific and Technical Information of China (English)

李珊珊; 徐志伟; 桑文文; 王伟英; 杨旭

2014-01-01

Objective To investigate the neuroprotective effect and possible mechanisms of Fucoidan ( FPS) in rats after cerebral ischemia-reperfusion injury. Methods A total of 48 rats were divided into sham group (n=12), mid-dle cerebral artery occlusion (MCAO group, n=12), low dose of FPS group (MCAO+FPS50 mg/kg) and high dose of FPS group (MCAO+FPS 100 mg/kg, n=12) according to random digits table method. The right common carotid artery and external carotid artery in rats of sham operation group were separated. In the cerebral ischemia-reperfusion injury group, low dose and high dose of FPS groups, middle cerebral artery occlusion models were made by suture method, and then FPS level dropped after reperfusion was given after ischemia for 2 h, and the FPS was injected via caudal veins with 50 and 100 mg/kg respectively in high dose of FPS group. All rats underwent nerve function evaluation by the Longa score of nerve behavior, the volume of cerebral infarction by TTC ( triphenyl tetrazolium chloride) method and the Nrf2 expression by Western blotting. Results Compared with those in the MCAO group, the nerve function scores in low dose and high dose of FPS groups were significantly reduced, and the Nrf2 expression levels were significantly increased. In high dose of FPS group, the changes of score and Nrf2 expression were more significant (P<0. 05, P<0. 01);while the volume of cerebral infarction was significantly reduced (P<0. 01). Conclusion FPS may protect nerves by raising the Nrf2 expression to reduce the volume of cerebral infarction in rats after cerebral ischemia-reperfusion injury.%目的：探讨褐藻多糖硫酸酯( FPS)对脑缺血再灌注损伤的神经保护作用及可能机制。方法将48只大鼠按照随机数字表法分为假手术组、大脑中动脉栓塞( MCAO)组、FPS低剂量组( MCAO+FPS 50 mg/kg)、FPS高剂量组( MCAO+FPS 100 mg/kg),每组12�

Financial impact of reducing door-to-balloon time in ST-elevation myocardial infarction: a single hospital experience.

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Khot, Umesh N; Johnson-Wood, Michele L; Geddes, Jason B; Ramsey, Curtis; Khot, Monica B; Taillon, Heather; Todd, Randall; Shaikh, Saeed R; Berg, William J

2009-07-26

The impact of reducing door-to-balloon time on hospital revenues, costs, and net income is unknown. We prospectively determined the impact on hospital finances of (1) emergency department physician activation of the catheterization lab and (2) immediate transfer of the patient to an immediately available catheterization lab by an in-house transfer team consisting of an emergency department nurse, a critical care unit nurse, and a chest pain unit nurse. We collected financial data for 52 consecutive ST-elevation myocardial infarction patients undergoing emergency percutaneous intervention from October 1, 2004-August 31, 2005 and compared this group to 80 consecutive ST-elevation myocardial infarction patients from September 1, 2005-June 26, 2006 after protocol implementation. Per hospital admission, insurance payments (hospital revenue) decreased ($35,043 +/- $36,670 vs. $25,329 +/- $16,185, P = 0.039) along with total hospital costs ($28,082 +/- $31,453 vs. $18,195 +/- $9,242, P = 0.009). Hospital net income per admission was unchanged ($6962 vs. $7134, P = 0.95) as the drop in hospital revenue equaled the drop in costs. For every $1000 reduction in total hospital costs, insurance payments (hospital revenue) dropped $1077 for private payers and $1199 for Medicare/Medicaid. A decrease in hospital charges ($70,430 +/- $74,033 vs. $53,514 +/- $23,378, P = 0.059), diagnosis related group relative weight (3.7479 +/- 2.6731 vs. 2.9729 +/- 0.8545, P = 0.017) and outlier payments with hospital revenue>$100,000 (7.7% vs. 0%, P = 0.022) all contributed to decreasing ST-elevation myocardial infarction hospitalization revenue. One-year post-discharge financial follow-up revealed similar results: Insurance payments: $49,959 +/- $53,741 vs. $35,937 +/- $23,125, P = 0.044; Total hospital costs: $39,974 +/- $37,434 vs. $26,778 +/- $15,561, P = 0.007; Net Income: $9984 vs. $9159, P = 0.855. All of the financial benefits of reducing door-to-balloon time in ST-elevation myocardial

Morphine reduces the threshold of helium preconditioning against myocardial infarction: the role of opioid receptors in rabbits

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Pagel, Paul S.; Krolikowski, John G.; Amour, Julien; Warltier, David C.; Weihrauch, Dorothee

2015-01-01

Objectives Brief, repetitive administration of helium before prolonged coronary artery occlusion and reperfusion protects myocardium against infarction. Opioid receptors mediate the cardioprotective effects of ischemic pre- and postconditioning, but whether these receptors also play a role in helium preconditioning is unknown. We tested the hypotheses that opioid receptors mediate helium preconditioning and that morphine (a μ1-opioid receptor agonist with δ1-opioid agonist properties) lowers the threshold of cardioprotection produced by helium in vivo. Design Randomized, prospective study. Setting University research laboratory. Participants Male New Zealand white rabbits. Interventions Rabbits (n=56) were instrumented for measurement of systemic hemodynamics and subjected to a 30 min left anterior descending coronary artery (LAD) occlusion and 3 h reperfusion. In separate experimental groups, rabbits (n=6 or 7 per group) received 0.9% saline (control), one or three cycles of 70% helium-30% oxygen administered for 5 min interspersed with 5 min of an air-oxygen mixture, morphine (0.1 mg/kg, i.v.), or the nonselective opioid antagonist naloxone (6 mg/kg, i.v.) before LAD occlusion. Other groups of rabbits received three cycles of helium or one cycle of helium plus morphine (0.1 mg/kg) in the absence or presence of naloxone (6 mg/kg) before ischemia and reperfusion. Statistical analysis of data was performed with analysis of variance for repeated measures followed by Bonferroni’s modification of Student’s t test. Measurements and Main Results Myocardial infarct size was determined using triphenyltetrazolium chloride staining and presented as a percentage of the left ventricular area at risk. Helium reduced myocardial infarct size in an exposure-related manner [36±6 (P>0.05) and 25±4% (P<0.05 versus control) for one and three cycles of helium, respectively; data are mean±SD] compared with control (44±7%). Morphine and naloxone alone did not affect infarct

Prognostic impact of physical activity prior to myocardial infarction

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Ejlersen, Hanne; Andersen, Zorana Jovanovic; von Euler-Chelpin, My Catarina

2017-01-01

the course of myocardial infarction by reducing case fatality and the subsequent risk of heart failure and mortality. Methods: A total of 14,223 participants in the Copenhagen City Heart Study were assessed at baseline in 1976-1978; 1,664 later developed myocardial infarction (mean age at myocardial...... estimated by logistic and Cox proportional hazards regression models, adjusted for age at myocardial infarction and other potential confounders. Results: A total of 425 (25.5%) myocardial infarctions were fatal. Higher levels of LTPA prior to myocardial infarction were associated with lower case fatality...

Transfusion of CXCR4-primed endothelial progenitor cells reduces cerebral ischemic damage and promotes repair in db/db diabetic mice.

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Ji Chen

Full Text Available This study investigated the role of stromal cell-derived factor-1α (SDF-1α/CXC chemokine receptor 4 (CXCR4 axis in brain and endothelial progenitor cells (EPCs, and explored the efficacy of CXCR4 primed EPCs in treating ischemic stroke in diabetes. The db/db diabetic and db/+ mice were used in this study. Levels of plasma SDF-1α and circulating CD34+CXCR4+ cells were measured. Brain SDF-1α and CXCR4 expression were quantified at basal and after middle cerebral artery occlusion (MCAO. In in vitro study, EPCs were transfected with adenovirus carrying null (Ad-null or CXCR4 (Ad-CXCR4 followed with high glucose (HG treatment for 4 days. For pathway block experiments, cells were pre-incubated with PI3K inhibitor or nitric oxide synthase (NOS inhibitor for two hours. The CXCR4 expression, function and apoptosis of EPCs were determined. The p-Akt/Akt and p-eNOS/eNOS expression in EPCs were also measured. In in vivo study, EPCs transfected with Ad-null or Ad-CXCR4 were infused into mice via tail vein. On day 2 and 7, the cerebral blood flow, neurologic deficit score, infarct volume, cerebral microvascular density, angiogenesis and neurogenesis were determined. We found: 1 The levels of plasma SDF-1α and circulating CD34+CXCR4+ cells were decreased in db/db mice; 2 The basal level of SDF-1α and MCAO-induced up-regulation of SDF-1α/CXCR4 axis were reduced in the brain of db/db mice; 3 Ad-CXCR4 transfection increased CXCR4 expression in EPCs and enhanced EPC colonic forming capacity; 4 Ad-CXCR4 transfection prevented EPCs from HG-induced dysfunction (migration and tube formation and apoptosis via activation of PI3K/Akt/eNOS signal pathway; 4 Ad-CXCR4 transfection enhanced the efficacy of EPC infusion in attenuating infarct volume and promoting angiogenesis and neurogenesis. Our data suggest that Ad-CXCR4 primed EPCs have better therapeutic effects for ischemia stroke in diabetes than unmodified EPCs do.

Effects of Sophora japonica flowers (Huaihua on cerebral infarction

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Hsieh Ching-Liang

2010-09-01

Full Text Available Abstract The dried flowers and buds of Sophora japonica are used as a medicinal herb in China, Japan and Korea to treat bleeding hemorrhoids and hematemesis. This article presents an overview of the effects of Sophora japonica on cerebral infarction based on literature searched from Medline, PubMed, Cochrane Library and the China National Knowledge Infrastructure (CNKI. Sophora japonica contains both anti-hemorrhagic and anti-hemostatic substances. Sophora japonica reduces cerebral infarction partly as a result of its anti-oxidative and anti-inflammatory activities. Previous studies found that Sophora japonica reduced the size of cerebral infarction and neurological deficits and reduced microglial activation, interleukin-1β release and number of apoptotic cells in ischemia-reperfusion injured Sprague-Dawley rats. Further study is required to determine the relationship between Sophora japonica-mediated reduction in cerebral infarction size and the effects of Sophora japonica on platelet aggregation and cardiovascular function.

Cerebral ischemic injury decreases α-synuclein expression in brain tissue and glutamate-exposed HT22 cells.

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Koh, Phil-Ok

2017-09-01

α-Synuclein is abundantly expressed in neuronal tissue, plays an essential role in the pathogenesis of neurodegenerative disorders, and exerts a neuroprotective effect against oxidative stress. Cerebral ischemia causes severe neurological disorders and neuronal dysfunction. In this study, we examined α-synuclein expression in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury and neuronal cells damaged by glutamate treatment. MCAO surgical operation was performed on male Sprague-Dawley rats, and brain samples were isolated 24 hours after MCAO. We confirmed neurological behavior deficit, infarction area, and histopathological changes following MCAO injury. A proteomic approach and Western blot analysis demonstrated a decrease in α-synuclein in the cerebral cortices after MCAO injury. Moreover, glutamate treatment induced neuronal cell death and decreased α-synuclein expression in a hippocampal-derived cell line in a dose-dependent manner. It is known that α-synuclein regulates neuronal survival, and low levels of α-synuclein expression result in cytotoxicity. Thus, these results suggest that cerebral ischemic injury leads to a reduction in α-synuclein and consequently causes serious brain damage.

Gastrodia and Uncaria (tianma gouteng) water extract exerts antioxidative and antiapoptotic effects against cerebral ischemia in vitro and in vivo.

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Xian, Jia Wen; Choi, Angus Yiu-Ting; Lau, Clara Bik-San; Leung, Wing Nang; Ng, Chun Fai; Chan, Chun Wai

2016-01-01

Gastrodia and Uncaria decoction (tianma gouteng yin) is commonly used in Chinese medicine to treat cerebral ischemia. The aim of this study was to investigate the neuroprotective effects of a water extract (GUW) of Gastrodia elata (tianma; GE) and Uncaria rhynchophylla (gouteng; UR) against ischemic insult using oxygen-glucose-deprived neuronal differentiated PC12 cells and rats subjected to middle cerebral artery occlusion (MCAO). GUW was prepared by boiling raw GE and UR in water, followed by the lyophilization of the resulting extract. Neuronal differentiated PC12 cells were subjected to oxygen-glucose deprivation with or without GUW. The neuroprotective effects of GUW were compared with those of the corresponding GE and UR extracts to tease apart the effects of the different herbs. The synergistic effect of GE and UR in GUW was measured using a modified version of Burgi's formulae. The neuroprotective mechanisms via Nrf2 and anti-apoptotic pathways were investigated using real time PCR and enzyme activity assays. The neuroprotective effects of GUW were studied in vivo using a rat MCAO model. Neurofunctional outcome and brain infarct volume we assessed. H&E staining, cresyl violet staining and immunohistochemistry were performed to assess the histological outcome. The results of lactate dehydrogenase assay showed that GUW protected cells in a concentration-dependent manner (P < 0.001). Moreover, the neuroprotective effects of GUW were greater than those of GE + UR (P = 0.018). Burgi's formula showed that the herbs in GUW acted synergistically to protect cells from ischemic injury. GUW significantly upregulated Bcl-2 expression (P = 0.0130) and reduced caspase-3 activity by 60 % (P < 0.001). GUW upregulated Nrf-2 expression (P = 0.0066) and the antioxidant response element pathway genes. The infarct volume was reduced by 55 % at day 7 of reperfusion (P < 0.001), and significant improvements were observed in the neurological deficit score and beam

Probucol plus cilostazol attenuate hypercholesterolemia‑induced exacerbation in ischemic brain injury via anti-inflammatory effects.

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Kim, Ji Hyun; Hong, Ki Whan; Bae, Sun Sik; Shin, Yong-Il; Choi, Byung Tae; Shin, Hwa Kyoung

2014-09-01

Probucol, a lipid-lowering agent with anti-oxidant properties, is involved in protection against atherosclerosis, while cilostazol, an antiplatelet agent, has diverse neuroprotective properties. In this study, we investigated the anti-inflammatory effects of probucol and cilostazol on focal cerebral ischemia with hypercholesterolemia. Apolipoprotein E (ApoE) knockout (KO) mice were fed a high-fat diet (HFD) with or without 0.3% probucol and/or 0.2% cilostazol for 10 weeks. To assess the protective effects of the combined therapy of probucol and cilostazol on ischemic injury, the mice received 40 min of middle cerebral artery occlusion (MCAO). Infarct volumes, neurobehavioral deficits and neuroinflammatory mediators were subsequently evaluated 48 h after reperfusion. Probucol alone and probucol plus cilostazol significantly decreased total- and low-density lipoprotein (LDL)-cholesterol in ApoE KO with HFD. MCAO resulted in significantly larger infarct volumes in ApoE KO mice provided with HFD compared to those fed a regular diet, although these volumes were significantly reduced in the probucol plus cilostazol group. Consistent with a smaller infarct size, probucol alone and the combined treatment of probucol and cilostazol improved neurological and motor function. In addition, probucol alone and probucol plus cilostazol decreased MCP-1 expression and CD11b and GFAP immuno-reactivity in the ischemic cortex. These findings suggested that the inhibitory effects of probucol plus cilostazol in MCP-1 expression in the ischemic brain with hypercholesterolemia allowed the identification of one of the mechanisms responsible for anti-inflammatory action. Probucol plus cilostazol may therefore serve as a therapeutic strategy for reducing the impact of stroke in hypercholesterolemic subjects.

Effects of Mesenchymal Stem Cell Treatment on the Expression of Matrix Metalloproteinases and Angiogenesis during Ischemic Stroke Recovery.

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Hyo Suk Nam

Full Text Available The efficacy of mesenchymal stem cell (MSC transplantation in ischemic stroke might depend on the timing of administration. We investigated the optimal time point of MSC transplantation. After MSC treatment, we also investigated the expression of matrix metalloproteinases (MMPs, which play a role in vascular and tissue remodeling.Human bone marrow-derived MSCs (2 × 10(6, passage 5 were administrated intravenously after permanent middle cerebral artery occlusion (MCAO was induced in male Sprague-Dawley rats. First, we determined the time point of MSC transplantation that led to maximal neurological recovery at 1 h, 1 day, and 3 days after MCAO. Next, we measured activity of MMP-2 and MMP-9, neurological recovery, infarction volume, and vascular density after transplanting MSCs at the time that led to maximal neurological recovery.Among the MSC-transplanted rats, those of the MSC 1-hour group showed maximal recovery in the rotarod test (P = 0.023 and the Longa score (P = 0.018. MMP-2 activity at 1 day after MCAO in the MSC 1-hour group was significantly higher than that in the control group (P = 0.002, but MMP-9 activity was not distinct. The MSC 1-hour group also showed smaller infarction volume and higher vascular density than did the control group.In a permanent model of rodent MCAO, very early transplantation of human MSCs (1 h after MCAO produced greater neurological recovery and decreased infraction volume. The elevation of MMP-2 activity and the increase in vascular density after MSC treatment suggest that MSCs might help promote angiogenesis and lead to neurological improvement during the recovery phase after ischemic stroke.

Intermittent fasting is neuroprotective in focal cerebral ischemia by minimizing autophagic flux disturbance and inhibiting apoptosis.

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Jeong, Ji Heun; Yu, Kwang Sik; Bak, Dong Ho; Lee, Je Hun; Lee, Nam Seob; Jeong, Young Gil; Kim, Dong Kwan; Kim, Jwa-Jin; Han, Seung-Yun

2016-11-01

Previous studies have demonstrated that autophagy induced by caloric restriction (CR) is neuroprotective against cerebral ischemia. However, it has not been determined whether intermittent fasting (IF), a variation of CR, can exert autophagy-related neuroprotection against cerebral ischemia. Therefore, the neuroprotective effect of IF was evaluated over the course of two weeks in a rat model of focal cerebral ischemia, which was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). Specifically, the role of autophagy modulation as a potential underlying mechanism for this phenomenon was investigated. It was demonstrated that IF reduced infarct volume and brain edema, improved neurobehavioral deficits, and rescued neuronal loss after MCAO/R. Furthermore, neuronal apoptosis was decreased by IF in the rat cortex. An increase in the number of autophagosomes (APs) was demonstrated in the cortices of IF-treated rats, using immunofluorescence staining and transmission electron microscopy. Using immunoblots, an IF-induced increase was detected in microtubule-associated protein 1 light chain 3 (LC3)-II, Rab7, and cathepsin D protein levels, which corroborated previous morphological studies. Notably, IF reduced the accumulation of APs and p62, demonstrating that IF attenuated the MCAO/R-induced disturbance of autophagic flux in neurons. The findings of the present study suggest that IF-induced neuroprotection in focal cerebral ischemia is due, at least in part, to the minimization of autophagic flux disturbance and inhibition of apoptosis.

Enhanced expressions of microvascular smooth muscle receptors after focal cerebral ischemia occur via the MAPK MEK/ERK pathway

DEFF Research Database (Denmark)

Maddahi, A.; Edvinsson, L.

2008-01-01

), the enhanced vascular receptor expression, and attenuated the cerebral infarct and improved neurology score. CONCLUSION: Our results show that MCAO results in upregulation of cerebrovascular ETB, AT1 and 5-HT1B receptors. Blockade of this event with a MEK1 inhibitor as late as 6 h after the insult reduced...... the role of the MEK/ERK pathway in receptor expression following ischemic brain injury using the specific MEK1 inhibitor U0126. METHODS AND RESULT: Rats were subjected to a 2-h middle cerebral artery occlusion (MCAO) followed by reperfusion for 48-h and the ischemic area was calculated. The expression...... of phosphorylated ERK1/2 and Elk-1, and of endothelin ETA and ETB, angiotensin AT1, and 5-hydroxytryptamine 5-HT1B receptors were analyzed with immunohistochemistry using confocal microscopy in cerebral arteries, microvessels and in brain tissue. The expression of endothelin ETB receptor was analyzed...

Parecoxib is neuroprotective in spontaneously hypertensive rats after transient middle cerebral artery occlusion: a divided treatment response?

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Kelsen, Jesper; Kjaer, Katrine; Chen, Gang; Pedersen, Michael; Røhl, Lisbeth; Frøkiaer, Jørgen; Nielsen, Søren; Nyengaard, Jens R; Rønn, Lars Christian B

2006-12-06

Anti-inflammatory treatment affects ischemic damage and neurogenesis in rodent models of cerebral ischemia. We investigated the potential benefit of COX-2 inhibition with parecoxib in spontaneously hypertensive rats (SHRs) subjected to transient middle cerebral artery occlusion (tMCAo). Sixty-four male SHRs were randomized to 90 min of intraluminal tMCAo or sham surgery. Parecoxib (10 mg/kg) or isotonic saline was administered intraperitoneally (IP) during the procedure, and twice daily thereafter. Nineteen animals were euthanized after 24 hours, and each hemisphere was examined for mRNA expression of pro-inflammatory cytokines and COX enzymes by quantitative RT-PCR. Twenty-three tMCAo animals were studied with diffusion and T2 weighted MRI within the first 24 hours, and ten of the SHRs underwent follow-up MRI six days later. Thirty-three SHRs were given 5-bromo-2'-deoxy-uridine (BrdU) twice daily on Day 4 to 7 after tMCAo. Animals were euthanized on Day 8 and the brains were studied with free-floating immunohistochemistry for activated microglia (ED-1), hippocampal granule cell BrdU incorporation, and neuronal nuclei (NeuN). Infarct volume estimation was done using the 2D nucleator and Cavalieri principle on NeuN-stained coronal brain sections. The total number of BrdU+ cells in the dentate gyrus (DG) of the hippocampus was estimated using the optical fractionator. We found a significant reduction in infarct volume in parecoxib treated animals one week after tMCAo (p < 0.03). Cortical ADC values in the parecoxib group were markedly less increased on Day 8 (p < 0.01). Interestingly, the parecoxib treated rats were segregated into two subgroups, suggesting a responder vs. non-responder phenomenon. We found indications of mRNA up-regulation of IL-1beta, IL-6, TNF-alpha and COX-2, whereas COX-1 remained unaffected. Hippocampal granule cell BrdU incorporation was not affected by parecoxib treatment. Presence of ED-1+ activated microglia in the hippocampus was related

The Effect of Photoluminescence of Bioceramic Irradiation on Middle Cerebral Arterial Occlusion in Rats

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Lei Zhang

2016-01-01

Full Text Available The purpose of this study is to determine the possible effect of photoluminescence of bioceramic (PLB on ischemic cerebral infarction (stroke, by using an animal model of transient middle cerebral artery occlusion (MCAO. Sprague-Dawley rats were used to induce MCAO to block the origin of the left MCAO; three months later, the positive chronic stroke rats were selected by running tunnel maze; the MCAO rats with significant chronic stroke and neurological defects were used for treadmill experiments with varying speed settings to test their capability for restoration after muscular fatigue under conditions of with and without PLB irradiation. As a result, PLB irradiation could improve exercise completion rate and average running speed during slow and fast treadmill settings. After PLB irradiation, the selected MCAO rats successfully completed all the second-round treadmill exercises at the maximum speed setting, and they had better restoration from muscular fatigue. An in vitro cell study on astrocytes of rats by bioceramic irradiation further demonstrated increased intracellular nitric oxide. To explain these results, we suggest that cortical brain stimulation of microcirculation and enhancement of peripheral muscular activity are the main causes of the improved exercise performance in MCAO rats by PLB.

Perillyl alcohol improves functional and histological outcomes against ischemia-reperfusion injury by attenuation of oxidative stress and repression of COX-2, NOS-2 and NF-κB in middle cerebral artery occlusion rats.

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Tabassum, Rizwana; Vaibhav, Kumar; Shrivastava, Pallavi; Khan, Andleeb; Ahmed, Mohd Ejaz; Ashafaq, Mohammad; Khan, M Badruzzaman; Islam, Farah; Safhi, Mohammed M; Islam, Fakhrul

2015-01-15

Perillyl alcohol (PA) is a monoterpene found in essential oils of mints, cherries, citreous fruits and lemon grass, reported to have antioxidant and anti-inflammatory properties. However, the role of PA in stroke is still illusive. Since oxidative stress and inflammation play a pivotal role in ischemia-reperfusion (I-R) injury, this study was designed to elucidate the potential effects of PA against I-R induced pathology in rat׳s brain. Middle cerebral artery occlusion (MCAO) for 2h followed by 22h reperfusion in Wistar male rats (250-280g, 14-16 weeks old) induced the behavioral and histological alterations along with exhausted antioxidant status and enhanced inflammatory mediators. However, PA administration (25, 50 and 100mg/kg b.wt orally once daily for 7 days) prior to MCAO significantly attenuated neurological deficits related to flexion test and spontaneous motor activity, improved grip strength and motor coordination in a dose dependent manner. PA treatment also inhibited oxidative stress in MCAO rats as evident from decreased lipid peroxidation and augmented level of reduced glutathione and restored activities of catalase, glutathione peroxidase, and glutathione reductase and thus, reduced infarct volume and protected the brain histology after I-R injury. Furthermore, PA markedly suppressed the level of proinflammatory cytokines (IL-1β, TNF α and IL-6) and down regulated expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (NOS-2) and nuclear factor κB (NF-κB) in MCAO group. In conclusion, PA mediates neuroprotection against I-R injury via mitigation of oxidative stress and inflammation and thus, may be a good therapeutic approach in stroke prone patient. Copyright © 2014 Elsevier B.V. All rights reserved.

Comparison of MSC-Neurogenin1 administration modality in MCAO rat model

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Shin Dong Hoon

2016-12-01

Full Text Available Intracerebral (IC grafting of mesenchymal stem cells (MSCs is not currently used in humans due to its potential complications. On the other hand, intra-arterial (IA administration can be facilitated for engrafting of intensifed MSCs in the injured human brain. The study is designed to compare the two methods of MSC administration using IA and IC routes through the parameters of behavior, infarct volume, cell distribution, and MSC identification. An ischemic stroke model was generated in Sprague Dawley male rats. This experiment used MSCs/Ngn1 that express Neurogenin1 (Ngn1 to ensure grafted MSC maintenance. MSCs/Ngn1 or normal saline was administrated via the IC or IA route on day 3. All animals were randomly assigned into four groups (five rats in each group: IC-control, IA-control, IC-MSCs/Ngn1, or IA-MSCs/Ngn1. Motor behaviors, infarct volume, and distribution of superparamagnetic iron oxide (SPIO-labeled cells on magnetic resonance imaging (MRI were compared from each group. There were no baseline differencess in motor behaviors or infarct volume between IC-MSCs/Ngn1 and IA-MSCs/Ngn1. Hovever, the IA-MSCs/Ngn1 group showed the greatest recovery on Rotarod testing and adhesive removal tests (p = 0.003 and p = 0.009 vs. IC-MSCs/Ngn1, respectively. The IA-MSCs/Ngn1 group also had more evenly distributed SPIO-labeled cells on MRI. The results suggest that IA administration is likely to be benefcial for humans based on its ability to improve behavioral outcomes and ensure even MSC engrafting.

Targeting immune co-stimulatory effects of PD-L1 and PD-L2 might represent an effective therapeutic strategy in stroke

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Sheetal eBodhankar

2014-08-01

Full Text Available Stroke outcome is worsened by the infiltration of inflammatory immune cells into ischemic brains. Our recent study demonstrated that PD-L1- and to a lesser extent PD-L2-deficient mice had smaller brain infarcts and fewer brain-infiltrating cells vs. WT mice, suggesting a pathogenic role for PD-Ligands in experimental stroke. We sought to ascertain PD-L1 and PD-L2-expressing cell types that affect T-cell activation, post-stroke in the context of other known co-stimulatory molecules. Thus, cells from male WT and PD-L-deficient mice undergoing 60 min of middle cerebral artery occlusion (MCAO followed by 96h of reperfusion were treated with neutralizing antibodies to study co-stimulatory and co-inhibitory interactions between CD80, CTLA-4, PD-1 and PD-Ls that regulate CD8+ and CD4+ T-cell activation. We found that antibody neutralization of PD-1 and CTLA-4 signaling post-MCAO resulted in higher proliferation in WT CD8+ and CD4+ T-cells, confirming an inhibitory role of PD-1 and CTLA-4 on T-cell activation. Also, CD80/CD28 interactions played a prominent regulatory role for the CD8+ T-cells and the PD-1/PD-L2 interactions were dominant in controlling the CD4+ T-cell responses in WT mice after stroke. A suppressive phenotype in PD-L1-deficient mice was attributed to CD80/CTLA-4 and PD-1/PD-L2 interactions. PD-L2 was crucial in modulating CD4+ T-cell responses, whereas PD-L1 regulated both CD8+ and CD4+ T-cells. To establish the contribution of PD-L1 and PD-L2 on regulatory B-cells (Bregs, infarct volumes were evaluated in male PD-L1- and PD-L2-deficient mice receiving IL-10+ B-cells 4h post-MCAO. PD-L2- but not PD-L1-deficient recipients of IL-10+ B-cells had markedly reduced infarct volumes, indicating a regulatory role of PD-L2 on Bregs. These results imply that PD-L1 and PD-L2 differentially control induction of T- and Breg-cell responses after MCAO, thus suggesting that selective targeting of PD-L1 and PD-L2 might represent a valuable therapeutic

Myocardial infarction in the conscious dog: three dimensional mapping of infarct, collateral flow and region at risk

International Nuclear Information System (INIS)

Jugdutt, B.I.; Hutchins, G.M.; Bulkley, B.H.; Becker, L.C.

1979-01-01

Myocardial infarcts were examined in dogs to determine the spatial distribution of infarction in the region at risk and the relation between infarction and collateral blood flow. Permanent occlusion of the left circumflex (LC) coronary artery at a constant site was made in 27 conscious dogs that were sacrificed 2 days later. The anatomic region at risk was defined by postmortem coronary arteriography as the volume of the occluded LC coronary bed. The masses of the left ventricle (LV), infarct (I) and risk region (R) were calculated from planimetered areas of weighted bread-loaf sections of LV. Infarct size was directly related to the mass of the risk region (I = 0.53 R - 9.87; r = 0.97; p < 0.001). There was no infarction when R was less than about 20 g or 20% of the LV. The infarcts were mainly subendocardial and tapered from base to apex of the LV; 34% of the risk region became infarcted at the base compared with 22% at the apex. In all dogs, a significant rim of noninfarcted myocardium was identified at lateral aspects of the risk region, even at the endocardial surface. Using 9-μ radioactive microspheres, initial postocclusion flow at the margin of the infarct, but well within the risk region, was higher than at the center, and outer flows were higher than inner flows. Postocclusion flow was even higher in the noninfarcted rim within the risk region, but was still significantly less than flow to normal, nonrisk areas. Collateral flows throughout the risk region increased during the first hour after occlusion, and were even higher at 2 days.Epicardially and laterally within the anatomic risk region there is a substantial amount of tissue that does not infarct despite initally reduced blood flow

Splenectomy reduces infarct volume and neuroinflammation in male but not female mice in experimental stroke

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Dotson, Abby L.; Wang, Jianming; Saugstad, Julie; Murphy, Stephanie J.; Offner, Halina

2014-01-01

The peripheral immune response contributes to neurodegeneration after stroke yet little is known about how this process differs between males and females. The current study demonstrates that splenectomy prior to experimental stroke eliminates sex differences in infarct volume and activated brain monocytes/microglia. In the periphery of both sexes, activated T cells correlate directly with stroke outcome while monocytes are reduced by splenectomy only in males. This study provides new information about the sex specific mechanisms of the peripheral immune response in neurodegeneration after stroke and demonstrates the need for representation of both sexes in basic and clinical stroke research. PMID:25434281

Novel Neurovascular Protective Agents: Effects of INV-155, INV-157, INV-159, and INV-161 versus Lipoic Acid and Captopril in a Rat Stroke Model

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Barry J. Connell

2012-01-01

Full Text Available Background. Lipoic acid (LA, which has significant antioxidant properties, may also function as a potent neuroprotectant. The synthetic compounds INV-155, INV-157, INV-159, and INV-161 are physiochemical combinations of lipoic acid and captopril. We sought to determine if these compounds have neuroprotective potential following middle cerebral artery occlusion (MCAO in rats. Methods. Male Sprague-Dawley rats were injected intravenously with captopril (1–50 mg/kg 30 minutes prior to MCAO. Blood pressure, heart rate, baroreceptor reflex sensitivity, and infarct size were measured. In addition, dose response effect on infarct size and cardiovascular parameters was determined using INV-155, INV-157, INV-159, and INV-161 and compared to captopril and LA. Results. Pretreatment with captopril and LA at all doses tested was neuroprotective. The compounds INV-159 (0.5–10 mg/kg and INV-161 (1–10 mg/kg produced a significant,dose-dependent decrease in infarct size. In contrast, INV-155 and INV-157 had no effect on infarct size. Conclusions. Combined pretreatment with captopril potentiated the neuroprotective benefit observed following LA alone. Both INV-159 and INV-161 were also neuroprotective. These results suggest that patients taking combinations of captopril and LA, either as combination therapy or in the form of INV-159 or INV-161, may also benefit from significant protection against cerebral infarction.

Pharmacologically increasing collateral perfusion during acute stroke using a carboxyhemoglobin gas transfer agent (Sanguinate™) in spontaneously hypertensive rats.

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Cipolla, Marilyn J; Linfante, Italo; Abuchowski, Abe; Jubin, Ronald; Chan, Siu-Lung

2018-05-01

Similar to patients with chronic hypertension, spontaneously hypertensive rats (SHR) develop fast core progression during middle cerebral artery occlusion (MCAO) resulting in large final infarct volumes. We investigated the effect of Sanguinate™ (SG), a PEGylated carboxyhemoglobin (COHb) gas transfer agent, on changes in collateral and reperfusion cerebral blood flow and brain injury in SHR during 2 h of MCAO. SG (8 mL/kg) or vehicle ( n = 6-8/group) was infused i.v. after 30 or 90 min of ischemia with 2 h reperfusion. Multi-site laser Doppler probes simultaneously measured changes in core MCA and collateral flow during ischemia and reperfusion using a validated method. Brain injury was measured using TTC. Animals were anesthetized with choral hydrate. Collateral flow changed little in vehicle-treated SHR during ischemia (-8 ± 9% vs. prior to infusion) whereas flow increased in SG-treated animals (29 ± 10%; p collateral flow in SHR during MCAO is consistent with small penumbra and large infarction. The ability to increase collateral flow in SHR with SG suggests that this compound may be useful as an adjunct to endovascular therapy and extend the time window for treatment.

Etiology, Localization and Prognosis in Cerebellar Infarctions

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Yavuz Yücel

2006-01-01

Full Text Available Cerebrovasculer disease are the most frequent disease of the brain. Cerebellar infarct remains % 1.5-4.2 of these diseases. Etiological factors, lesion localization, symptoms and findings and relationship with prognosis of our patients with cerebellar infarct were investigated in our study. For this purpose, 32 patients were evaluated who were admitted to the Dicle University Medical School Department of Neurology in 1995-2001 hospitalized with the diagnosis of clinically and radiological confirmed cerebellar infarction.All of patients in the study group, 21 (%65.6 were male and 11 (%34.3 female. Age of overall patients ranged between 40 and 75 years with a mean of 57.8±10.2 years. Atherothrombotic infarct was the most frequent reason at the etiologic clinical classification. The most frequently found localization was the posterior inferior cerebellar artery infarct (%50. The leading two risk factors were hypertension (%78.1 and cigarette smoking (%50. The most common sign and symptoms were vertigo (%93.7, vomiting (%75, headache (%68.7 and cerebellar dysfunction findings (%50. The mean duration of hospitalization was 16.3±7.6 days. Overall mortality rate was found to be % 6.2. Finally, the most remarkable risk factors at cerebellar infarct patients are hypertension and atherosclerosis at etiology. We are considering that, controlling of these factors will reduce the appearance frequency of cerebellar infarcts.

Signaling factors in stem cell-mediated repair of infarcted myocardium

NARCIS (Netherlands)

Vandervelde, S; van Luyn, MJA; Tio, RA; Harmsen, MC

Myocardial infarction leads to scar formation and subsequent reduced cardiac performance. The ultimate therapy after myocardial infarction would pursue stem cell-based regeneration. The aim of stem cell-mediated cardiac repair embodies restoration of cardiac function by regeneration of healthy

Danshen-Chuanxiong-Honghua Ameliorates Cerebral Impairment and Improves Spatial Cognitive Deficits after Transient Focal Ischemia and Identification of Active Compounds

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Xianhua Zhang

2017-07-01

Full Text Available Previously, we only apply a traditional Chinese medicine (TCM Danshen-Chuanxiong-Honghua (DCH for cardioprotection via anti-inflammation in rats of acute myocardial infarction by occluding coronary artery. Presently, we select not only DCH but also its main absorbed compound ferulic acid (FA for cerebra protection via similar action of mechanism above in animals of the transient middle cerebral artery occlusion (tMCAO. We investigated whether oral administration of DCH and FA could ameliorate MCAO-induced brain lesions in animals. By using liquid chromatography-tandem mass spectrometry (LC-MS/MS, we analyzed four compounds, including tanshinol, salvianolic acid B, hydroxysafflor yellow A and especially FA as the putative active components of DCH extract in the plasma, cerebrospinal fluid and injured hippocampus of rats with MCAO. In our study, it was assumed that FA played a similar neuroprotective role to DCH. We found that oral pretreatment with DCH (10 or 20 g/kg and FA (100 mg/kg improved neurological function and alleviated the infarct volume as well as brain edema in a dose-dependent manner. These changes were accompanied by improved ischemia-induced apoptosis and decreased the inflammatory response. Additionally, chronic treatment with DCH reversed MCAO-induced spatial cognitive deficits in a manner associated with enhanced neurogenesis and increased the expression of brain-derived neurotrophic factor in lesions of the hippocampus. These findings suggest that DCH has the ability to recover cognitive impairment and offer neuroprotection against cerebral ischemic injury via inhibiting microenvironmental inflammation and triggering of neurogenesis in the hippocampus. FA could be one of the potential active compounds.

Prevention and intervention studies with telmisartan, ramipril and their combination in different rat stroke models.

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Christa Thoene-Reineke

Full Text Available OBJECTIVES: The effects of AT1 receptor blocker, telmisartan, and the ACE inhibitor, ramipril, were tested head-to head and in combination on stroke prevention in hypertensive rats and on potential neuroprotection in acute cerebral ischemia in normotensive rats. METHODS: Prevention study: Stroke-prone spontaneously hypertensive rats (SHR-SP were subjected to high salt and randomly assigned to 4 groups: (1 untreated (NaCl, n = 24, (2 telmisartan (T; n = 27, (3 ramipril (R; n = 27 and (4 telmisartan + ramipril (T+R; n = 26. Drug doses were selected to keep blood pressure (BP at 150 mmHg in all groups. Neurological signs and stroke incidence at 50% mortality of untreated SHR-SP were investigated. Intervention study: Normotensive Wistar rats were treated s.c. 5 days prior to middle cerebral artery occlusion (MCAO for 90 min with reperfusion. Groups (n = 10 each: (1 sham, (2 vehicle (V; 0.9% NaCl, (3 T (0.5 mg/kg once daily, (4 R (0.01 mg/kg twice daily, (5 R (0.1 mg/kg twice daily or (6 T (0.5 mg/kg once daily plus R (0.01 mg/kg twice daily. Twenty-four and 48 h after MCAO, neurological outcome (NO was determined. Forty-eight h after MCAO, infarct volume by MRI, neuronal survival, inflammation factors and neurotrophin receptor (TrkB were analysed. RESULTS: Stroke incidence was reduced, survival was prolonged and neurological outcome was improved in all treated SHR-SP with no differences between treated groups. In the acute intervention study, T and T+R, but not R alone, improved NO, reduced infarct volume, inflammation (TNFα, and induced TrkB receptor and neuronal survival in comparison to V. CONCLUSIONS: T, R or T+R had similar beneficial effects on stroke incidence and NO in hypertensive rats, confirming BP reduction as determinant factor in stroke prevention. In contrast, T and T+R provided superior neuroprotection in comparison to R alone in normotensive rats with induced cerebral ischemia.

Hyperglycemia decreases expression of 14-3-3 proteins in an animal model of stroke.

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Jeon, Seong-Jun; Sung, Jin-Hee; Koh, Phil-Ok

2016-07-28

Diabetes is a severe metabolic disorder and a major risk factor for stroke. Stroke severity is worse in patients with diabetes compared to the non-diabetic population. The 14-3-3 proteins are a family of conserved acidic proteins that are ubiquitously expressed in cells and tissues. These proteins are involved in many cellular processes including metabolic pathways, signal transduction, protein trafficking, protein synthesis, and cell cycle control. This study investigated 14-3-3 proteins expression in the cerebral cortex of animals with diabetes, cerebral ischemic injury and a combination of both diabetes and cerebral ischemic injury. Diabetes was induced by intraperitoneal injection of streptozotocin (40mg/kg) in adult male rats. After 4 weeks of treatment, middle cerebral artery occlusion (MCAO) was performed for the induction of focal cerebral ischemia and cerebral cortex tissue was collected 24h after MCAO. We confirmed that diabetes increases infarct volume following MCAO compared to non-diabetic animals. In diabetic animals with MCAO injury, reduction of 14-3-3 β/α, 14-3-3 ζ/δ, 14-3-3 γ, and 14-3-3 ε isoforms was detected. The expression of these proteins was significantly decreased in diabetic animals with MCAO injury compared to diabetic-only and MCAO-only animals. Moreover, Western blot analysis ascertained the decreased expression of 14-3-3 family proteins in diabetic animals with MCAO injury, including β/α, ζ/δ, γ, ε, τ, and η isoforms. These results show the changes of 14-3-3 proteins expression in streptozotocin-induced diabetic animals with MCAO injury. Thus, these findings suggest that decreases in 14-3-3 proteins might be involved in the regulation of 14-3-3 proteins under the presence of diabetes following MCAO. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Neuroprotective effect of electroacupuncture and upregulation of hypoxia-inducible factor-1α during acute ischaemic stroke in rats.

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Li, Ce; Zhang, Tingting; Yu, Kewei; Xie, Hongyu; Bai, Yulong; Zhang, Li; Wu, Yi; Wang, Nianhong

2017-10-01

Acupuncture is a traditional method that has been widely used in various fields of medicine with therapeutic effect. However, evidence of effectiveness to support the application of electroacupuncture (EA) during the process of ischaemia is scarce. To investigate dynamic changes in hypoxia-inducible factor (HIF)-1α expression as well as its association with neurological status in rats subjected to acute ischaemic stroke and EA intervention. Forty adult male rats were randomly divided into three groups that received sham surgery (Control group, n=10) or underwent middle cerebral artery occlusion and EA (MCAO+EA group, n=15) or minimal acupuncture as a control treatment (MCAO+MA group, n=15). The rats in the MCAO+EA and MCAO+MA groups received EA or acupuncture without any electrical current, respectively, during 90 min of ischaemia. Rats in the Control group received the same surgical procedure but without MCAO. EA involved electrical stimulation of needles inserted into the quadriceps at 50 Hz frequency and 3 mA current intensity. Neurological status was evaluated on postoperative day 1, and cerebral infarction volume (IV) and HIF-1α expression 24 hours later. Neurological scores were improved and cerebral IV was decreased in the MCAO+EA group compared to the MCAO+MA group (both p<0.05). Moreover, HIF-1α expression was higher in the MCAO+EA group versus the MCAO+MA group (p<0.05). EA enhanced recovery of neurological function, decreased cerebral IV and increased HIF-1α expression in ischaemic rats. Further research is needed to determine whether EA is effective for stroke treatment through the stimulation of muscle contraction. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

Zingiber officinale Mitigates Brain Damage and Improves Memory Impairment in Focal Cerebral Ischemic Rat

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Wattanathorn, Jintanaporn; Jittiwat, Jinatta; Tongun, Terdthai; Muchimapura, Supaporn; Ingkaninan, Kornkanok

2011-01-01

Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect of Zingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO). Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia. PMID:21197427

Zingiber officinale Mitigates Brain Damage and Improves Memory Impairment in Focal Cerebral Ischemic Rat

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Jintanaporn Wattanathorn

2011-01-01

Full Text Available Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect of Zingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO. Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA, superoxide dismutase (SOD, catalase (CAT, and glutathione peroxidase (GSH-Px in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia.

Chronic ischemic mitral regurgitation and papillary muscle infarction detected by late gadolinium-enhanced cardiac magnetic resonance imaging in patients with ST-segment elevation myocardial infarction

NARCIS (Netherlands)

Bouma, Wobbe; Willemsen, Hendrik M.; Lexis, Chris P. H.; Prakken, Niek H.; Lipsic, Erik; van Veldhuisen, Dirk J.; Mariani, Massimo A.; van der Harst, Pim; van der Horst, Iwan C. C.

2016-01-01

Both papillary muscle infarction (PMI) and chronic ischemic mitral regurgitation (CIMR) are associated with reduced survival after myocardial infarction. The influence of PMI on CIMR and factors influencing both entities are incompletely understood. We sought to determine the influence of PMI on

Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction: results of a multicenter, randomized, placebo-controlled trial: the Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial.

Science.gov (United States)

Mahaffey, K W; Puma, J A; Barbagelata, N A; DiCarli, M F; Leesar, M A; Browne, K F; Eisenberg, P R; Bolli, R; Casas, A C; Molina-Viamonte, V; Orlandi, C; Blevins, R; Gibbons, R J; Califf, R M; Granger, C B

1999-11-15

The Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial was designed to test the hypothesis that adenosine as an adjunct to thrombolysis would reduce myocardial infarct size. Reperfusion therapy for acute myocardial infarction (MI) has been shown to reduce mortality, but reperfusion itself also may have deleterious effects. The AMISTAD trial was a prospective, open-label trial of thrombolysis with randomization to adenosine or placebo in 236 patients within 6 h of infarction onset. The primary end point was infarct size as determined by Tc-99 m sestamibi single-photon emission computed tomography (SPECT) imaging 6+/-1 days after enrollment based on multivariable regression modeling to adjust for covariates. Secondary end points were myocardial salvage index and a composite of in-hospital clinical outcomes (death, reinfarction, shock, congestive heart failure or stroke). In all, 236 patients were enrolled. Final infarct size was assessed in 197 (83%) patients. There was a 33% relative reduction in infarct size (p = 0.03) with adenosine. There was a 67% relative reduction in infarct size in patients with anterior infarction (15% in the adenosine group vs. 45.5% in the placebo group) but no reduction in patients with infarcts located elsewhere (11.5% for both groups). Patients randomized to adenosine tended to reach the composite clinical end point more often than those assigned to placebo (22% vs. 16%; odds ratio, 1.43; 95% confidence interval, 0.71 to 2.89). Many agents thought to attenuate reperfusion injury have been unsuccessful in clinical investigation. In this study, adenosine resulted in a significant reduction in infarct size. These data support the need for a large clinical outcome trial.

Inhibition of CXCL12 signaling attenuates the postischemic immune response and improves functional recovery after stroke

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Ruscher, Karsten; Kuric, Enida; Liu, Yawei

2013-01-01

cell-derived factor-1 (CXCL12). To mimic beneficial effects of EE, we studied the impact of inhibiting CXCL12 action on functional recovery after transient MCAO (tMCAO). Rats treated with the specific CXCL12 receptor antagonist 1-[4-(1,4,8,11-tetrazacyclotetradec-1-ylmethyl)phenyl]methyl]-1......After stroke, brain inflammation in the ischemic hemisphere hampers brain tissue reorganization and functional recovery. Housing rats in an enriched environment (EE) dramatically improves recovery of lost neurologic functions after experimental stroke. We show here that rats housed in EE after......,4,8,11-tetrazacyclo-tetradecan (AMD3100) showed improved recovery compared with saline-treated rats after tMCAO, without a concomitant reduction in infarct size. This was accompanied by a reduction of infiltrating immune cells in the ischemic hemisphere, particularly cluster of differentiation 3-positive (CD3...

Justification for intravenous magnesium therapy in acute myocardial infarction

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Rasmussen, H S

1988-01-01

Recent studies have shown that patients with acute myocardial infarction (AMI) are magnesium-deficient and develop an additional transient decrease in serum magnesium concentrations (S-Mg c) during the acute phase of the infarct. Animal experiments, as well as studies on humans, have indicated.......v. magnesium therapy on mortality and incidence of arrhythmias in patients with AMI has been evaluated. Magnesium treatment more than halved the acute mortality and incidence of arrhythmias requiring treatment in three of the four intervention studies. The mechanisms behind the beneficial effect of magnesium...... therapy are probably multifactorial; a direct depressive effect on the cardiac conducting system; a peripheral dilatory effect on the arteries, reducing the afterload on the myocardium; a reduced infarct size; an ion-stabilizing effect, maintaining stable intra and extracellular concentrations...

Defibrotide reduces infarct size in a rabbit model of experimental myocardial ischaemia and reperfusion.

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Thiemermann, C.; Thomas, G. R.; Vane, J. R.

1989-01-01

1. Defibrotide, a single-stranded polydeoxyribonucleotide obtained from bovine lungs, has significant anti-thrombotic, pro-fibrinolytic and prostacyclin-stimulating properties. 2. The present study was designed to evaluate the effects of defibrotide on infarct size and regional myocardial blood flow in a rabbit model of myocardial ischaemia and reperfusion. 3. Defibrotide (32 mg kg-1 bolus + 32 mg kg-1 h-1, i.v.) either with or without co-administration of indomethacin (5 mg kg-1 x 2, i.v.) was administered 5 min after occlusion of the left anterior-lateral coronary artery and continued during the 60 min occlusion and subsequent 3 h reperfusion periods. 4. Defibrotide significantly attenuated the ischaemia-induced ST-segment elevation and abolished the reperfusion-related changes (R-wave reduction and Q-wave development) in the electrocardiogram. In addition, defibrotide significantly improved myocardial blood flow in normal and in ischaemic, but not in infarcted sections of the heart. The improvement in blood flow in normal perfused myocardium, but not in the ischaemic area was prevented by indomethacin. 5. Although the area at risk was similar in all animal groups studied, defibrotide treatment resulted in a 51% reduction of infarct size. Indomethacin treatment abolished the reduction of infarct size seen with defibrotide alone. 6. The data demonstrate a considerable cardioprotective effect of defibrotide in the reperfused ischaemic rabbit myocardium. This effect may be related, at least in part, to a stimulation of endogenous prostaglandin formation. Other possible mechanisms are discussed. PMID:2758223

Right ventricular function after acute myocardial infarction: dependence upon infarct related coronary artery

International Nuclear Information System (INIS)

Cho, Ihn Ho; Chun, Kyung A; Won, Kyu Chang; Lee, Hyung Woo; Hong, Geu Ru; Park, Jong Seon; Shin, Dong Gu; Kim, Young Jo; Shim, Bong Sub

2004-01-01

We studied to know the relation between right ventricular function and infarct-related artery after acute myocardial infarction. The right and left ventricular function after a first myocardial infarction was assessed ECG-gated blood pool single photon emission computed tomography (GBPS) algorithms (Cedars-Sinai Medical Center, Los Angels, Calif) (12 after LAD related infarction (group 1) and 15 after RCA related infarction (group 2)). The left ventricular ejection fraction, end-diastolic volume and end-systolic volume did not differ significantly between two groups( group 1 vs 2 :LVEF 50.8% vs 55.1%. LVEDV=73.2 vs 79.7 ml, LVESV=38 vs 44 ml : P>0.05), but right ventricular ejection fraction, end-diastolic volume and end-systolic volume were significantly different after anterior myocardial infarction between two groups( group 1 vs 2 : RVEF=57.3% vs 46.3%. RVEDV=56.4 vs 95.1 ml, RVESV=25.6 vs 54.6ml : P<0.05). There was evidence of right ventricular dilatation in the group with RCA related infarction. Six with inferior infarction had abnormal right ventricular ejection fractions (< 40%). The relation between right and left ventricular ejection fractions was markedly different in the two groups. In the group with RCA related infarction there was a significant linear relation between right and left ventricular ejection fraction(R=0.5). Whereas in the group with LAD related infarction there was not (R=-0.3). Thus right ventricular dysfunction commonly occurs after RCA related infarction. Right ventricular impairment is related after RCA related infarction, but are independent after LAD related infarction. Finally, the different effects of LAD and RCA related infarction on right ventricular function may be explained by site of the myocardial wall involvement after infarction

Enhanced cerebrovascular expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 via the MEK/ERK pathway during cerebral ischemia in the rat

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Maddahi Aida

2009-06-01

Full Text Available Abstract Background Cerebral ischemia is usually characterized by a reduction in local blood flow and metabolism and by disruption of the blood-brain barrier in the infarct region. The formation of oedema and opening of the blood-brain barrier in stroke is associated with enhanced expression of metalloproteinase-9 (MMP-9 and tissue inhibitor of metalloproteinase-1 (TIMP-1. Results Here, we found an infarct volume of 24.8 ± 2% and a reduced neurological function after two hours of middle cerebral artery occlusion (MCAO, followed by 48 hours of recirculation in rat. Immunocytochemistry and confocal microscopy revealed enhanced expression of MMP-9, TIMP-1, and phosphorylated ERK1/2 in the smooth muscle cells of the ischemic MCA and associated intracerebral microvessels. The specific MEK1/2 inhibitor U0126, given intraperitoneal zero or 6 hours after the ischemic event, reduced the infarct volume significantly (11.8 ± 2% and 14.6 ± 3%, respectively; P Conclusion These data are the first to show that the elevated vascular expression of MMP-9 and TIMP-1, associated with breakdown of the blood-brain barrier following focal ischemia, are transcriptionally regulated via the MEK/ERK pathway.

Differential effects of tissue plasminogen activator and streptokinase on infarct size and on rate of enzyme release: influence of early infarct related artery patency : The GUSTO Enzyme Substudy

NARCIS (Netherlands)

T. Baardman (Taco); W.T. Hermens (Wim); G.P. Molhoek; G. Grollier (Gilles); M.E. Pfisterer (Matthias); M.L. Simoons (Maarten); T. Lenderink (Timo)

1996-01-01

textabstractBACKGROUND: The recent international GUSTO trial of 41,021 patients with acute myocardial infarction demonstrated improved 90-min infarct related artery patency as well as reduced mortality in patients treated with an accelerated regimen of tissue plasminogen activator, compared to

Cerebroprotective Effect of Moringa oleifera against Focal Ischemic Stroke Induced by Middle Cerebral Artery Occlusion

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Woranan Kirisattayakul

2013-01-01

Full Text Available The protection against ischemic stroke is still required due to the limitation of therapeutic efficacy. Based on the role of oxidative stress in stroke pathophysiology, we determined whether Moringa oleifera, a plant possessing potent antioxidant activity, protected against brain damage and oxidative stress in animal model of focal stroke. M. oleifera leaves extract at doses of 100, 200 and 400 mg·kg−1 was orally given to male Wistar rats (300–350 g once daily at a period of 2 weeks before the occlusion of right middle cerebral artery (Rt.MCAO and 3 weeks after Rt.MCAO. The determinations of neurological score and temperature sensation were performed every 7 days throughout the study period, while the determinations of brain infarction volume, MDA level, and the activities of SOD, CAT, and GSH-Px were performed 24 hr after Rt.MCAO. The results showed that all doses of extract decreased infarction volume in both cortex and subcortex. The protective effect of medium and low doses of extract in all areas occurred mainly via the decreased oxidative stress. The protective effect of the high dose extract in striatum and hippocampus occurred via the same mechanism, whereas other mechanisms might play a crucial role in cortex. The detailed mechanism required further exploration.

The Long-Term Outcome Comparison of Different Time-Delayed Kallikrein Treatments in a Mouse Cerebral Ischemic Model

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Yaohui Ni

2018-01-01

Full Text Available Delayed administration of kallikrein after cerebral infarction can improve neurological function. However, the appropriate kallkrein treatment time after ischemic stroke has not been illuminated. In this study, we compared the long-term outcome among three kallikrein therapeutic regimens starting at different time points following mouse cerebral ischemia. Furthermore, the protective mechanisms involving neurogenesis, angiogenesis, and AKT-GSK3β-VEGF signaling pathway were analyzed. Human tissue kallikrein was injected through the tail vein daily starting at 8 h, 24 h, or 36 h after right middle cerebral artery occlusion (MCAO until the 28th day. Three therapeutic regimens all protected against neurological dysfunction, but kallikrein treatment starting at 8 h after MCAO had the best efficacy. Additionally, kallikrein treatment at 8 h after MCAO significantly enhanced cell proliferation including neural stem cell and induced differentiation of neural stem cell into mature neuron. Kallikrein treatment starting at 8 h also promoted more angiogenesis than other two treatment regimens, which was associated with AKT-GSK3β-VEGF signaling pathway. Thus, we confirm that three delayed kallikrein treatments provide protection against cerebral infarction and furthermore suggest that kallikrein treatment starting at 8 h had a better effect than that at 24 h and 36 h. These findings provide the experimental data contributing to better clinical application of exogenous kallikrein.

A comparison of long-term functional outcome after 2 middle cerebral artery occlusion models in rats.

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Roof, R L; Schielke, G P; Ren, X; Hall, E D

2001-11-01

Proven behavioral assessment strategies for testing potential therapeutic agents in rat stroke models are needed. Few studies include tasks that demand higher levels of sensorimotor and cognitive function. Because behavioral outcome and rate of recovery vary among ischemia models, there is a need to characterize and compare performance on specific tasks across models. To this end, sensorimotor and cognitive deficits were assessed during a 5-week period after either permanent proximal middle cerebral artery occlusion (pMCAO) or permanent distal middle cerebral artery occlusion combined with a 90-minute occlusion of both common carotid arteries (dMCAO/tCCAO) in Sprague-Dawley rats. The EBST, hindlimb and forelimb placing, and cylinder tests were given at regular intervals postinjury to assess sensorimotor function. Cognitive function was assessed with a multitrial water navigation task. pMCAO, which caused both striatal and cortical damage, produced persistent sensorimotor and cognitive deficits. Limb placing responses and postural reflexes were impaired throughout the month of testing. A persistent bias for using the ipsilateral forelimb for wall movements in the cylinder test was observed as well as a bias for landing on the opposite forelimb. pMCAO rats were also impaired in the water navigation task. dMCAO/tCCAO, which caused only cortical damage, produced similar sensorimotor deficits, but these were greatly diminished by 2 weeks after injury. No impairment was found for water tank navigation. Correlations between forelimb placing (both models), water navigation performance (pMCAO model), and sensorimotor asymmetry (dMCAOtCCAO model) and infarct volume were observed. Based on the range of functions affected and stability of observed deficits, the pMCAO model appears to be preferable to the dMCAO/tCCAO model for use in assessing therapeutic agents for stroke.

Prolonged preconditioning with natural honey against myocardial infarction injuries.

Science.gov (United States)

Eteraf-Oskouei, Tahereh; Shaseb, Elnaz; Ghaffary, Saba; Najafi, Moslem

2013-07-01

Potential protective effects of prolonged preconditioning with natural honey against myocardial infarction were investigated. Male Wistar rats were pre-treated with honey (1%, 2% and 4%) for 45 days then their hearts were isolated and mounted on a Langendorff apparatus and perfused with a modified Krebs-Henseleit solution during 30 min regional ischemia fallowed by 120 min reperfusion. Two important indexes of ischemia-induced damage (infarction size and arrhythmias) were determined by computerized planimetry and ECG analysis, respectively. Honey (1% and 2%) reduced infarct size from 23±3.1% (control) to 9.7±2.4 and 9.5±2.3%, respectively (Phoney (1%) significantly reduced (PHoney (1% and 2%) also significantly decreased number of ventricular ectopic beats (VEBs). In addition, incidence and duration of reversible ventricular fibrillation (Rev VF) were lowered by honey 2% (Phoney produced significant reduction in the incidences of VT, total and Rev VF, duration and number of VT. The results showed cardioprotective effects of prolonged pre-treatment of rats with honey following myocardial infarction. Maybe, the existence of antioxidants and energy sources (glucose and fructose) in honey composition and improvement of hemodynamic functions may involve in those protective effects.

Trandolapril reduces the incidence of atrial fibrillation after acute myocardial infarction in patients with left ventricular dysfunction

DEFF Research Database (Denmark)

Pedersen, O D; Bagger, H; Køber, Lars Valeur

1999-01-01

in patients with reduced left ventricular function secondary to acute myocardial infarction. The patients in this study were those who qualified for inclusion into the TRAndolapril Cardiac Evaluation (TRACE) study, a randomized double-blind placebo-controlled study and who had sinus rhythm on the ECG obtained...... at randomization. Patients who fulfilled the criteria for inclusion were randomized to treatment with the ACE inhibitor trandolapril or placebo and were followed up for 2 to 4 years. Development and time to occurrence of atrial fibrillation in one 12-lead ECG recorded at the outpatient visits was the primary end...

Oxidized calmodulin kinase II regulates conduction following myocardial infarction: a computational analysis.

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Matthew D Christensen

2009-12-01

Full Text Available Calmodulin kinase II (CaMKII mediates critical signaling pathways responsible for divergent functions in the heart including calcium cycling, hypertrophy and apoptosis. Dysfunction in the CaMKII signaling pathway occurs in heart disease and is associated with increased susceptibility to life-threatening arrhythmia. Furthermore, CaMKII inhibition prevents cardiac arrhythmia and improves heart function following myocardial infarction. Recently, a novel mechanism for oxidative CaMKII activation was discovered in the heart. Here, we provide the first report of CaMKII oxidation state in a well-validated, large-animal model of heart disease. Specifically, we observe increased levels of oxidized CaMKII in the infarct border zone (BZ. These unexpected new data identify an alternative activation pathway for CaMKII in common cardiovascular disease. To study the role of oxidation-dependent CaMKII activation in creating a pro-arrhythmia substrate following myocardial infarction, we developed a new mathematical model of CaMKII activity including both oxidative and autophosphorylation activation pathways. Computer simulations using a multicellular mathematical model of the cardiac fiber demonstrate that enhanced CaMKII activity in the infarct BZ, due primarily to increased oxidation, is associated with reduced conduction velocity, increased effective refractory period, and increased susceptibility to formation of conduction block at the BZ margin, a prerequisite for reentry. Furthermore, our model predicts that CaMKII inhibition improves conduction and reduces refractoriness in the BZ, thereby reducing vulnerability to conduction block and reentry. These results identify a novel oxidation-dependent pathway for CaMKII activation in the infarct BZ that may be an effective therapeutic target for improving conduction and reducing heterogeneity in the infarcted heart.

Comparison of outcomes after hospitalization for worsening heart failure, myocardial infarction, and stroke in patients with heart failure and reduced and preserved ejection fraction

DEFF Research Database (Denmark)

Kristensen, Søren L; Jhund, Pardeep S; Køber, Lars

2015-01-01

AIMS: To investigate the prognostic significance of hospitalization for worsening heart failure (WHF), myocardial infarction (MI), and stroke in patients with chronic heart failure (HF). METHODS AND RESULTS: We studied 5011 patients with HF and reduced EF (HF-REF) in the CORONA trial and 4128...

Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial.

Science.gov (United States)

Hofmeijer, Jeannette; Kappelle, L Jaap; Algra, Ale; Amelink, G Johan; van Gijn, Jan; van der Worp, H Bart

2009-04-01

Patients with space-occupying hemispheric infarctions have a poor prognosis, with case fatality rates of up to 80%. In a pooled analysis of randomised trials, surgical decompression within 48 h of stroke onset reduced case fatality and improved functional outcome; however, the effect of surgery after longer intervals is unknown. The aim of HAMLET was to assess the effect of decompressive surgery within 4 days of the onset of symptoms in patients with space-occupying hemispheric infarction. Patients with space-occupying hemispheric infarction were randomly assigned within 4 days of stroke onset to surgical decompression or best medical treatment. The primary outcome measure was the modified Rankin scale (mRS) score at 1 year, which was dichotomised between good (0-3) and poor (4-6) outcome. Other outcome measures were the dichotomy of mRS score between 4 and 5, case fatality, quality of life, and symptoms of depression. Analysis was by intention to treat. This trial is registered, ISRCTN94237756. Between November, 2002, and October, 2007, 64 patients were included; 32 were randomly assigned to surgical decompression and 32 to best medical treatment. Surgical decompression had no effect on the primary outcome measure (absolute risk reduction [ARR] 0%, 95% CI -21 to 21) but did reduce case fatality (ARR 38%, 15 to 60). In a meta-analysis of patients in DECIMAL (DEcompressive Craniectomy In MALignant middle cerebral artery infarction), DESTINY (DEcompressive Surgery for the Treatment of malignant INfarction of the middle cerebral arterY), and HAMLET who were randomised within 48 h of stroke onset, surgical decompression reduced poor outcome (ARR 16%, -0.1 to 33) and case fatality (ARR 50%, 34 to 66). Surgical decompression reduces case fatality and poor outcome in patients with space-occupying infarctions who are treated within 48 h of stroke onset. There is no evidence that this operation improves functional outcome when it is delayed for up to 96 h after stroke onset

Lack of macrophage migration inhibitory factor in mice does not affect hallmarks of the inflammatory/immune response during the first week after stroke

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Deierborg Tomas

2011-06-01

Full Text Available Abstract Background Macrophage migration inhibitory factor (MIF has been proposed to play a detrimental role in stroke. We recently showed that MIF promotes neuronal death and aggravates neurological deficits during the first week after experimental stroke, in mice. Since MIF regulates tissue inflammation, we studied the putative role of MIF in post-stroke inflammation. Methods We subjected C57BL/6 mice, Mif-/- (MIF-KO or Mif+/+ (WT, to a transient occlusion of the right middle cerebral artery (tMCAo or sham-surgery. We studied MIF expression, GFAP expression and the number of CD74-positive cells in the ischemic brain hemisphere 7 days after tMCAo using primarily immunohistochemistry. We determined IFN-γ, IL-2, IL-4, IL-5, IL-10, IL-12, KC/CXCL-1 and TNF-α protein levels in the brain (48 h after surgery and serum (48 h and 7 days after surgery by a multiplex immunoassay. Results We observed that MIF accumulates in neurons and astrocytes of the peri-infarct region, as well as in microglia/macrophages of the infarct core up to 7 days after stroke. Among the inflammatory mediators analyzed, we found a significant increase in cerebral IL-12 and KC levels after tMCAo, in comparison to sham-surgery. Importantly, the deletion of Mif did not significantly affect the levels of the cytokines evaluated, in the brain or serum. Moreover, the spleen weight 48 h and 7 days subsequent to tMCAo was similar in WT and MIF-KO mice. Finally, the extent of GFAP immunoreactivity and the number of MIF receptor (CD74-positive cells within the ischemic brain hemisphere did not differ significantly between WT and MIF-KO mice subjected to tMCAo. Conclusions We conclude that MIF does not affect major components of the inflammatory/immune response during the first week after experimental stroke. Based on present and previous evidence, we propose that the deleterious MIF-mediated effects in stroke depend primarily on an intraneuronal and/or interneuronal action.

High-intensity training reduces intermittent hypoxia-induced ER stress and myocardial infarct size.

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Bourdier, Guillaume; Flore, Patrice; Sanchez, Hervé; Pepin, Jean-Louis; Belaidi, Elise; Arnaud, Claire

2016-01-15

Chronic intermittent hypoxia (IH) is described as the major detrimental factor leading to cardiovascular morbimortality in obstructive sleep apnea (OSA) patients. OSA patients exhibit increased infarct size after a myocardial event, and previous animal studies have shown that chronic IH could be the main mechanism. Endoplasmic reticulum (ER) stress plays a major role in the pathophysiology of cardiovascular disease. High-intensity training (HIT) exerts beneficial effects on the cardiovascular system. Thus, we hypothesized that HIT could prevent IH-induced ER stress and the increase in infarct size. Male Wistar rats were exposed to 21 days of IH (21-5% fraction of inspired O2, 60-s cycle, 8 h/day) or normoxia. After 1 wk of IH alone, rats were submitted daily to both IH and HIT (2 × 24 min, 15-30m/min). Rat hearts were either rapidly frozen to evaluate ER stress by Western blot analysis or submitted to an ischemia-reperfusion protocol ex vivo (30 min of global ischemia/120 min of reperfusion). IH induced cardiac proapoptotic ER stress, characterized by increased expression of glucose-regulated protein kinase 78, phosphorylated protein kinase-like ER kinase, activating transcription factor 4, and C/EBP homologous protein. IH-induced myocardial apoptosis was confirmed by increased expression of cleaved caspase-3. These IH-associated proapoptotic alterations were associated with a significant increase in infarct size (35.4 ± 3.2% vs. 22.7 ± 1.7% of ventricles in IH + sedenary and normoxia + sedentary groups, respectively, P < 0.05). HIT prevented both the IH-induced proapoptotic ER stress and increased myocardial infarct size (28.8 ± 3.9% and 21.0 ± 5.1% in IH + HIT and normoxia + HIT groups, respectively, P = 0.28). In conclusion, these findings suggest that HIT could represent a preventive strategy to limit IH-induced myocardial ischemia-reperfusion damages in OSA patients. Copyright © 2016 the American Physiological Society.

Arctigenin protects focal cerebral ischemia-reperfusion rats through inhibiting neuroinflammation.

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Fan, Tao; Jiang, Wei Long; Zhu, Jian; Feng Zhang, Yu

2012-01-01

Stroke is the third leading cause of death in industrialized countries and the most important cause of acquired adult disability. Many evidences suggest that inflammation accounts for the progression of cerebral ischemic injury. Arctigenin, a phenylpropanoid dibenzylbutyrolactone lignin isolated from certain plants, has shown anti-inflammatory activity against diabetes and Alzheimer's disease. In this study, we tested whether arctigenin can protect middle cerebral artery occluded (MCAO) rats. Male Sprague-Dawley rats were pretreated with arctigenin or vehicle for 7 d before being subjected to transient occlusion of middle cerebral artery and reperfusion. Rats were evaluated at 24 h after MCAO for neurological deficit scoring. Furthermore, the mechanism of the anti-inflammatory effect of arctigenin was investigated with a focus on inflammatory cells, proinflammatory cytokines, and transcriptional factors. Arctigenin significantly reduced cerebral infarction and improved neurological outcome. Arctigenin suppressed the activation of microglia and decreased the expression of interleukin (IL)- 1β and tumor necrosis factor (TNF)-α. These results revealed that arctigenin has a promising therapeutic effect in ischemic stroke treatment through an anti-inflammatory mechanism.

Neuroprotective effect of Buddleja officinalis extract on transient middle cerebral artery occlusion in rats.

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Lee, Dae-Hee; Ha, Nina; Bu, Yung-Min; Choi, Hyoung Il; Park, Yoo Guen; Kim, Yoon Bum; Kim, Mi-Yeon; Kim, Hocheol

2006-08-01

The flower buds of Buddleja officinalis MAXIM (Loganiaceae) are used to treat headache and inflammatory diseases in traditional Korean medicine. In the present study, the neuroprotective effects of the methanolic extract of B. officinalis (BOME) and of its hexane fraction (BOHF) were investigated in a middle cerebral artery occlusion (MCAo, 120 min occlusion, 24 h reperfusion) Sprague-Dawley rat model. BOME or BOHF (100 mg/kg, p.o.) was twice administered 30 min before the onset of MCAo and 2 h after reperfusion. BOME and BOHF treated groups showed infarct volumes reduced by 33.9% and 68.2%, respectively, at 2 h occlusion. In BOHF treated animals, cyclooxygenase-2 and iNOS inductions were inhibited in ischemic hemispheres at both the mRNA and protein levels. Furthermore, in vitro studies showed that BOME and BOHF both inhibited LPS-induced nitric oxide production in BV-2 mouse microglial cells. These results suggest that the anti-inflammatory and the microglial activation inhibitory effects of B. officinalis extract may contribute to its neuroprotective effects in brain ischemia.

High Prestroke Physical Activity Is Associated with Reduced Infarct Growth in Acute Ischemic Stroke Patients Treated with Intravenous tPA and Randomized to Remote Ischemic Perconditioning

DEFF Research Database (Denmark)

Blauenfeldt, Rolf Ankerlund; Hougaard, Kristina D; Mouridsen, Kim

2017-01-01

A high prestroke physical activity (PA) level is associated with reduced stroke rate, stroke mortality, better functional outcome, and possible neuroprotective abilities. The aim of the present study was to examine the possible neuroprotective effect of prestroke PA on 24-h cerebral infarct growth...... admission) PA was quantified using the PA Scale for the Elderly (PASE) questionnaire at baseline. Infarct growth was evaluated using MRI (acute, 24-h, and 1-month). PASE scores were obtained from 102 of 153 (67%) patients with a median (interquartile range) age of 66 (58-73) years. A high prestroke PA level...

Dysfunctional nitric oxide signalling increases risk of myocardial infarction.

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Erdmann, Jeanette; Stark, Klaus; Esslinger, Ulrike B; Rumpf, Philipp Moritz; Koesling, Doris; de Wit, Cor; Kaiser, Frank J; Braunholz, Diana; Medack, Anja; Fischer, Marcus; Zimmermann, Martina E; Tennstedt, Stephanie; Graf, Elisabeth; Eck, Sebastian; Aherrahrou, Zouhair; Nahrstaedt, Janja; Willenborg, Christina; Bruse, Petra; Brænne, Ingrid; Nöthen, Markus M; Hofmann, Per; Braund, Peter S; Mergia, Evanthia; Reinhard, Wibke; Burgdorf, Christof; Schreiber, Stefan; Balmforth, Anthony J; Hall, Alistair S; Bertram, Lars; Steinhagen-Thiessen, Elisabeth; Li, Shu-Chen; März, Winfried; Reilly, Muredach; Kathiresan, Sekar; McPherson, Ruth; Walter, Ulrich; Ott, Jurg; Samani, Nilesh J; Strom, Tim M; Meitinger, Thomas; Hengstenberg, Christian; Schunkert, Heribert

2013-12-19

Myocardial infarction, a leading cause of death in the Western world, usually occurs when the fibrous cap overlying an atherosclerotic plaque in a coronary artery ruptures. The resulting exposure of blood to the atherosclerotic material then triggers thrombus formation, which occludes the artery. The importance of genetic predisposition to coronary artery disease and myocardial infarction is best documented by the predictive value of a positive family history. Next-generation sequencing in families with several affected individuals has revolutionized mutation identification. Here we report the segregation of two private, heterozygous mutations in two functionally related genes, GUCY1A3 (p.Leu163Phefs*24) and CCT7 (p.Ser525Leu), in an extended myocardial infarction family. GUCY1A3 encodes the α1 subunit of soluble guanylyl cyclase (α1-sGC), and CCT7 encodes CCTη, a member of the tailless complex polypeptide 1 ring complex, which, among other functions, stabilizes soluble guanylyl cyclase. After stimulation with nitric oxide, soluble guanylyl cyclase generates cGMP, which induces vasodilation and inhibits platelet activation. We demonstrate in vitro that mutations in both GUCY1A3 and CCT7 severely reduce α1-sGC as well as β1-sGC protein content, and impair soluble guanylyl cyclase activity. Moreover, platelets from digenic mutation carriers contained less soluble guanylyl cyclase protein and consequently displayed reduced nitric-oxide-induced cGMP formation. Mice deficient in α1-sGC protein displayed accelerated thrombus formation in the microcirculation after local trauma. Starting with a severely affected family, we have identified a link between impaired soluble-guanylyl-cyclase-dependent nitric oxide signalling and myocardial infarction risk, possibly through accelerated thrombus formation. Reversing this defect may provide a new therapeutic target for reducing the risk of myocardial infarction.

Comparing patients with spinal cord infarction and cerebral infarction: clinical characteristics, and short-term outcome

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Naess H

2011-08-01

Full Text Available Halvor Naess, Fredrik RomiDepartment of Neurology, Haukeland University Hospital, N-5021 Bergen, NorwayBackground: To compare the clinical characteristics, and short-term outcome of spinal cord infarction and cerebral infarction.Methods: Risk factors, concomitant diseases, neurological deficits on admission, and short-term outcome were registered among 28 patients with spinal cord infarction and 1075 patients with cerebral infarction admitted to the Department of Neurology, Haukeland University Hospital, Bergen, Norway. Multivariate analyses were performed with location of stroke (cord or brain, neurological deficits on admission, and short-term outcome (both Barthel Index [BI] 1 week after symptom onset and discharge home or to other institution as dependent variables.Results: Multivariate analysis showed that patients with spinal cord infarction were younger, more often female, and less afflicted by hypertension and cardiac disease than patients with cerebral infarction. Functional score (BI was lower among patients with spinal cord infarctions 1 week after onset of symptoms (P < 0.001. Odds ratio for being discharged home was 5.5 for patients with spinal cord infarction compared to cerebral infarction after adjusting for BI scored 1 week after onset (P = 0.019.Conclusion: Patients with spinal cord infarction have a risk factor profile that differs significantly from that of patients with cerebral infarction, although there are some parallels to cerebral infarction caused by atherosclerosis. Patients with spinal cord infarction were more likely to be discharged home when adjusting for early functional level on multivariate analysis.Keywords: spinal cord infarction, cerebral infarction, risk factors, short-term outcome

Mechanism of Mitochondrial Connexin43′s Protection of the Neurovascular Unit under Acute Cerebral Ischemia-Reperfusion Injury

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Shuai Hou

2016-05-01

Full Text Available We observed mitochondrial connexin43 (mtCx43 expression under cerebral ischemia-reperfusion (I/R injury, analyzed its regulation, and explored its protective mechanisms. Wistar rats were divided into groups based on injections received before middle cerebral artery occlusion (MCAO. Cerebral infarction volume was detected by 2,3,5-triphenyltetrazolim chloride staining, and cell apoptosis was observed by transferase dUTP nick end labeling. We used transmission electron microscopy to observe mitochondrial morphology and determined superoxide dismutase (SOD activity and malondialdehyde (MDA content. MtCx43, p-mtCx43, protein kinase C (PKC, and p-PKC expression were detected by Western blot. Compared with those in the IR group, cerebral infarction volumes in the carbenoxolone (CBX and diazoxide (DZX groups were obviously smaller, and the apoptosis indices were down-regulated. Mitochondrial morphology was damaged after I/R, especially in the IR and 5-hydroxydecanoic acid (5-HD groups. Similarly, decreased SOD activity and increased MDA were observed after MCAO; CBX, DZX, and phorbol-12-myristate-13-acetate (PMA reduced mitochondrial functional injury. Expression of mtCx43 and p-mtCx43 and the p-Cx43/Cx43 ratio were significantly lower in the IR group than in the sham group. These abnormalities were ameliorated by CBX, DZX, and PMA. MtCx43 may protect the neurovascular unit from acute cerebral IR injury via PKC activation induced by mitoKATP channel agonists.

A protective role of early collateral blood flow in patients with ST-segment elevation myocardial infarction.

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Kim, Eun Kyoung; Choi, Jin-Ho; Song, Young Bin; Hahn, Joo-Yong; Chang, Sung-A; Park, Sung-Ji; Lee, Sang-Chol; Choi, Seung-Hyuk; Choe, Yeon Hyeon; Park, Seung Woo; Gwon, Hyeon-Cheol

2016-01-01

Conflict persists regarding whether the presence of early collateral blood flow to the infarct-related artery has an effective role in reducing infarct size and improving myocardial salvage in patients with ST-segment elevation myocardial infarction (STEMI). We sought to investigate the impact of the collateral circulation on myocardial salvage and infarct size in STEMI patients. In 306 patients who were diagnosed with STEMI and underwent cardiac magnetic resonance within 1 week after revascularization, initial collateral flow to the infarct-related artery was assessed by coronary angiography. Using cardiac magnetic resonance imaging, myocardial infarct size and salvage were measured. Among 247 patients with preprocedural Thrombolysis in Myocardial Infarction flow 0/1, 54 (22%) patients had good collaterals (Rentrop grade ≥ 2, Collateral Connection Score ≥ 2). Infarct size and area at risk were significantly smaller in patients with good collaterals than those with poor collaterals (infarct size: 17.1 ± 10.1 %LV vs 21.8 ± 10.5 %LV, P = .003, area at risk: 33.8 ± 16.8 %LV vs 38.8 ± 15.5 %LV, P = .039). There was a significant difference of myocardial salvage index between 2 groups (50.9% ± 15.0% vs 43.8% ± 18.5%, P = .005). Poor collateralization was an independent predictor for large infarct size (odd ratio 2.48 [1.28-4.80], P = .007). In patients with STEMI, the presence of well-developed collaterals to occluded coronary artery from the noninfarct vessel and its extent were independently associated with reduced infarct burden and improved myocardial salvage. Our results help explain why MI patients with well-developed collateralization have reduced mortality and morbidity. Copyright © 2015 Elsevier Inc. All rights reserved.

CT features of renal infarction

International Nuclear Information System (INIS)

Suzer, Okan; Shirkhoda, Ali; Jafri, S. Zafar; Madrazo, Beatrice L.; Bis, Kostaki G.; Mastromatteo, James F.

2002-01-01

Purpose: To demonstrate the different patterns of renal infarction to avoid pitfalls. To present 'flip-flop enhancement' pattern in renal infarction. Materials and methods: Retrospective review of a total of 41 renal infarction in 37 patients were done. These patients underwent initial CT and the diagnosis of renal infarction was confirmed with either follow up CT or at surgery. Results: Twenty-three patients had wedge-shaped focal infarcts, nine patients had global and five patients had multifocal infarcts of the kidneys. Cortical rim sign was seen predominantly with global infarcts. In five patients, a 'flip-flop enhancement' pattern was observed. In two patients, planned renal biopsies due to tumefactive renal lesions were cancelled because of 'flip-flop enhancement' pattern on follow up CTs. Conclusion: Although most of our cases were straightforward for the diagnosis of renal infarction, cases with tumefactive lesions and global infarctions without the well-known cortical rim sign were particularly challenging. We describe a new sign, flip-flop enhancement pattern, which we believe solidified the diagnosis of renal infarction in five of our cases. The authors recommend further investigations for association of flip-flop enhancement and renal infarction

Effect of ligustrazine on levels of amino acid neurotransmitters in rat striatum after cerebral ischemia-reperfusion injury.

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Han, Jin; Wan, Hai-Tong; Yang, Jie-Hong; Zhang, Yu-Yan; Ge, Li-Jun; Bie, Xiao-Dong

2014-01-01

This study aimed to evaluate the effect of ligustrazine on levels of amino acid transmitters in the extracellular fluid of striatum following cerebral ischemia/reperfusion (I/R) in male Sprague-Dawley rats. A microdialysis cannula guide was implanted into the right striatum. After recovery, animals underwent a sham operation or middle cerebral artery occlusion (MCAO). Those that developed cerebral ischemia after MCAO were randomized to receive propylene glycol salt water and ligustrazine respectively. Striatal fluid samples were collected from all animals at 15-min intervals after treatment and were subjected to HPLC analysis of aspartic acid, glutamic acid, taurine, and γ-amino butyric acid. Upon the last sample collection, animals were sacrificed and brain tissue specimens were collected for triphenyltetrazolium chloride staining and NeuN staining. Compared with the sham operation, MCAO induced significant neurological deficits and increased striatal concentrations of the four neurotransmitters assessed in a time-dependent manner (P cerebral infarction-protective agent may have potential clinical implications for I/R-related brain damage.

Relaxin reduces susceptibility to post-infarct atrial fibrillation in mice due to anti-fibrotic and anti-inflammatory properties

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Beiert, Thomas; Tiyerili, Vedat; Knappe, Vincent

2017-01-01

Background Relaxin-2 (RLX) is a peptide hormone that exerts beneficial anti-fibrotic and anti-inflammatory effects in diverse models of cardiovascular disease. The goal of this study was to determine the effects of RLX treatment on the susceptibility to atrial fibrillation (AF) after myocardial...... infarction (MI). Methods Mice with cryoinfarction of the left anterior ventricular wall were treated for two weeks with either RLX (75 μg/kg/d) or vehicle (sodium acetate) delivered via subcutaneously implanted osmotic minipumps. Results RLX treatment significantly attenuated the increase in AF......-inducibility following cryoinfarction and reduced the mean duration of AF episodes. Furthermore, epicardial mapping of both atria revealed an increase in conduction velocity. In addition to an attenuation of atrial hypertrophy, chronic application of RLX reduced atrial fibrosis, which was linked to a significant...

Reduced infarct size in neuroglobin-null mice after experimental stroke in vivo

DEFF Research Database (Denmark)

Raida, Zindy; Hundahl, Christian Ansgar; Kelsen, Jesper

2012-01-01

Neuroglobin is considered to be a novel important pharmacological target in combating stroke and neurodegenerative disorders, although the mechanism by which this protection is accomplished remains an enigma. We hypothesized that if neuroglobin is directly involved in neuroprotection, then perman......, then permanent cerebral ischemia would lead to larger infarct volumes in neuroglobin-null mice than in wild-type mice....

Neuronal Rho GTPase Rac1 elimination confers neuroprotection in a mouse model of permanent ischemic stroke.

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Karabiyik, Cansu; Fernandes, Rui; Figueiredo, Francisco Rosário; Socodato, Renato; Brakebusch, Cord; Lambertsen, Kate Lykke; Relvas, João Bettencourt; Santos, Sofia Duque

2017-09-28

The Rho GTPase Rac1 is a multifunctional protein involved in distinct pathways ranging from development to pathology. The aim of the present study was to unravel the contribution of neuronal Rac1 in regulating the response to brain injury induced by permanent focal cerebral ischemia (pMCAO). Our results show that pMCAO significantly increased total Rac1 levels in wild type mice, mainly through rising nuclear Rac1, while a reduction in Rac1 activation was observed. Such changes preceded cell death induced by excitotoxic stress. Pharmacological inhibition of Rac1 in primary neuronal cortical cells prevented the increase in oxidative stress induced after overactivation of glutamate receptors. However, this was not sufficient to prevent the associated neuronal cell death. In contrast, RNAi-mediated knock down of Rac1 in primary cortical neurons prevented cell death elicited by glutamate excitotoxicity and decreased the activity of NADPH oxidase. To test whether in vivo down regulation of neuronal Rac1 was neuroprotective after pMCAO, we used tamoxifen-inducible neuron-specific conditional Rac1-knockout mice. We observed a significant 50% decrease in brain infarct volume of knockout mice and a concomitant increase in HIF-1α expression compared to littermate control mice, demonstrating that ablation of Rac1 in neurons is neuroprotective. Transmission electron microscopy performed in the ischemic brain showed that lysosomes in the infarct of Rac1- knockout mice were preserved at similar levels to those of non-infarcted tissue, while littermate mice displayed a decrease in the number of lysosomes, further corroborating the notion that Rac1 ablation in neurons is neuroprotective. Our results demonstrate that Rac1 plays important roles in the ischemic pathological cascade and that modulation of its levels is of therapeutic interest. © 2017 International Society of Neuropathology.

Diet-Induced Ketosis Protects Against Focal Cerebral Ischemia in Mouse.

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Xu, Kui; Ye, Lena; Sharma, Katyayini; Jin, Yongming; Harrison, Matthew M; Caldwell, Tylor; Berthiaume, Jessica M; Luo, Yu; LaManna, Joseph C; Puchowicz, Michelle A

2017-01-01

Over the past decade we have consistently shown that ketosis is neuroprotective against ischemic insults in rats. We reported that diet-induced ketotic rats had a significant reduction in infarct volume when subjected to middle cerebral artery occlusion (MCAO), and improved survival and recovery after cardiac arrest and resuscitation. The neuroprotective mechanisms of ketosis (via ketogenic diet; KG) include (i) ketones are alternate energy substrates that can restore energy balance when glucose metabolism is deficient and (ii) ketones modulate cell-signalling pathways that are cytoprotective. We investigated the effects of diet-induced ketosis following transient focal cerebral ischemia in mice. The correlation between levels of ketosis and hypoxic inducible factor-1alpha (HIF-1α), AKT (also known as protein kinase B or PKB) and 5' AMP-activated protein kinase (AMPK) were determined. Mice were fed with KG diet or standard lab-chow (STD) diet for 4 weeks. For the MCAO group, mice underwent 60 min of MCAO and total brain infarct volumes were evaluated 48 h after reperfusion. In a separate group of mice, brain tissue metabolites, levels of HIF-1α, phosphorylated AKT (pAKT), and AMPK were measured. After feeding a KG diet, levels of blood ketone bodies (beta-hydroxyburyrate, BHB) were increased. There was a proportional decrease in infarct volumes with increased blood BHB levels (KG vs STD; 4.2 ± 0.6 vs 7.8 ± 2.2 mm 3 , mean ± SEM). A positive correlation was also observed with HIF-1α and pAKT relative to blood BHB levels. Our results showed that chronic ketosis can be induced in mice by KG diet and was neuroprotective against focal cerebral ischemia in a concentration dependent manner. Potential mechanisms include upregulation of cytoprotective pathways such as those associated with HIF-1α, pAKT and AMPK.

Anterior ST depression with acute transmural inferior infarction due to posterior infarction. A vectorcardiographic and scintigraphic study

International Nuclear Information System (INIS)

Mukharji, J.; Murray, S.; Lewis, S.E.; Croft, C.H.; Corbett, J.R.; Willerson, J.T.; Rude, R.E.

1984-01-01

The hypothesis that anterior ST segment depression represents concomitant posterior infarction was tested in 49 patients admitted with a first transmural inferior myocardial infarction. Anterior ST depression was defined as 0.1 mV or more ST depression in leads V1, V2 or V3 on an electrocardiogram recorded within 18 hours of infarction. Serial vectorcardiograms and technetium pyrophosphate scans were obtained. Eighty percent of the patients (39 of 49) had anterior ST depression. Of these 39 patients, 34% fulfilled vectorcardiographic criteria for posterior infarction, and 60% had pyrophosphate scanning evidence of posterior infarction. Early anterior ST depression was neither highly sensitive (84%) nor specific (20%) for the detection of posterior infarction as defined by pyrophosphate imaging. Of patients with persistent anterior ST depression (greater than 72 hours), 87% had posterior infarction detected by pyrophosphate scan. In patients with inferior myocardial infarction, vectorcardiographic evidence of posterior infarction correlated poorly with pyrophosphate imaging data. Right ventricular infarction was present on pyrophosphate imaging in 40% of patients with pyrophosphate changes of posterior infarction but without vectorcardiographic evidence of posterior infarction. It is concluded that: 1) the majority of patients with acute inferior myocardial infarction have anterior ST segment depression; 2) early anterior ST segment depression in such patients is not a specific marker for posterior infarction; and 3) standard vectorcardiographic criteria for transmural posterior infarction may be inaccurate in patients with concomitant transmural inferior myocardial infarction or right ventricular infarction, or both

Lycium barbarum Extracts Protect the Brain from Blood-Brain Barrier Disruption and Cerebral Edema in Experimental Stroke

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Yang, Di; Li, Suk-Yee; Yeung, Chung-Man; Chang, Raymond Chuen-Chung; So, Kwok-Fai; Wong, David; Lo, Amy C. Y.

2012-01-01

Background and Purpose Ischemic stroke is a destructive cerebrovascular disease and a leading cause of death. Yet, no ideal neuroprotective agents are available, leaving prevention an attractive alternative. The extracts from the fruits of Lycium barbarum (LBP), a Chinese anti-aging medicine and food supplement, showed neuroprotective function in the retina when given prophylactically. We aim to evaluate the protective effects of LBP pre-treatment in an experimental stroke model. Methods C57BL/6N male mice were first fed with either vehicle (PBS) or LBP (1 or 10 mg/kg) daily for 7 days. Mice were then subjected to 2-hour transient middle cerebral artery occlusion (MCAO) by the intraluminal method followed by 22-hour reperfusion upon filament removal. Mice were evaluated for neurological deficits just before sacrifice. Brains were harvested for infarct size estimation, water content measurement, immunohistochemical analysis, and Western blot experiments. Evans blue (EB) extravasation was determined to assess blood-brain barrier (BBB) disruption after MCAO. Results LBP pre-treatment significantly improved neurological deficits as well as decreased infarct size, hemispheric swelling, and water content. Fewer apoptotic cells were identified in LBP-treated brains by TUNEL assay. Reduced EB extravasation, fewer IgG-leaky vessels, and up-regulation of occludin expression were also observed in LBP-treated brains. Moreover, immunoreactivity for aquaporin-4 and glial fibrillary acidic protein were significantly decreased in LBP-treated brains. Conclusions Seven-day oral LBP pre-treatment effectively improved neurological deficits, decreased infarct size and cerebral edema as well as protected the brain from BBB disruption, aquaporin-4 up-regulation, and glial activation. The present study suggests that LBP may be used as a prophylactic neuroprotectant in patients at high risk for ischemic stroke. PMID:22438957

Respiratory muscle endurance is limited by lower ventilatory efficiency in post-myocardial infarction patients

OpenAIRE

Neves,Laura M. T.; Karsten,Marlus; Neves,Victor R.; Beltrame,Thomas; Borghi-Silva,Audrey; Catai,Aparecida M.

2014-01-01

Background: Reduced respiratory muscle endurance (RME) contributes to increased dyspnea upon exertion in patients with cardiovascular disease. Objective: The objective was to characterize ventilatory and metabolic responses during RME tests in post-myocardial infarction patients without respiratory muscle weakness. Method: Twenty-nine subjects were allocated into three groups: recent myocardial infarction group (RG, n=9), less-recent myocardial infarction group (LRG, n=10), and contr...

Statins and perioperative myocardial infarction. | Levin | Southern ...

African Journals Online (AJOL)

The growing prevalence of atherosclerosis means that perioperative myocardial infarction (PMI) is of significant concern to anesthesiologists. Perioperative revascularization (if indicated medically), beta blockade (in high risk patients) and statin therapy are therapeutic modalities that are currently employed to reduce PMI.

MANAGEMENT OF DIABETES IN ACUTE MYOCARDIAL INFARCTION IN CELJE GENERAL HOSPITAL IN 1999

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Gregor Veninšek

2001-12-01

Full Text Available Background. DIGAMI study showed that intrahospital mortality and mortality at one year after myocardial infarction can be significantly reduced in diabetics treated in acute phase of myocardial infarction by GI infusion and afterwards for at least three months with intensive insulin treatment. Mortality can be reduced for more than 50% in a subgroup of patients younger than 70 years, without congestive heart failure, with first myocardial infarction, not treated with insulin or digitalis. In this perspective we reviewed treatment of diabetics with acute myocardial infarction in 1999 in Celje General Hospital.Methods. We reviewed documentation of treatment of all diabetics with acute myocardial infarction treated in Celje General Hospital in 1999. We collected data on number of newly discovered diabetes, on previous treatment of diabetes, on treatment of diabetes during hospitalization and at discharge, on drugs used for treatment of diabetes and on mortality during hospitalization.Results. Diabetics presented 20% of all patients with acute myocardial infarction treated in Celje General Hospital in 1999. None of patients received GI infusion, none had intensively managed blood sugar. 24% of patients were treated with sulfonylureas in acute phase of myocardial infarction. 33% of patients were discharged from hospital with insulin therapy. Intrahospital mortality was 9%, comparable with patients without diabetes.Conclusions. In 1999 was intrahospital treatment of diabetics with acute myocardial infarction in Celje General Hospital successful as their intrahospital mortality equaled non-diabetics. Treatment of diabetes itself, during hospitalization and after discharge, on the other hand, in 1999 had not been up to date according to results of recent studies. In our opinion, it is mandatory for diabetologist to make part of the team that treats diabetic with acute myocardial infarction

Application of radionuclide infarct scintigraphy to diagnose perioperative myocardial infarction following revascularization

International Nuclear Information System (INIS)

Klausner, S.C.; Botvinick, E.H.; Shames, D.; Ullyot, D.J.; Fishman, N.H.; Roe, B.B.; Ebert, P.A.; Chatterjee, K.; Parmley, W.W.

1977-01-01

To evaluate the application of radionuclide infarct scintigraphy to diagnose myocardial infarction after revascularization, we obtained postoperative technetium 99m pyrophosphate myocardial scintigrams, serial electrocardiograms and CPK-MB isoenzymes in ten control and 51 revascularized patients. All control patients had negative electrocardiograms and scintigrams, but eight had positive isoenzymes. Eight revascularized patients had positive electrocardiograms, images and enzymes and two had positive scintigrams and enzymes with negative electrocardiograms. Thirty-four patients with negative electrocardiograms and scintigrams had positive isoenzymes; in only seven patients were all tests negative. Our data suggest radionuclide infarct scintigraphy is a useful adjunct to the electrocardiogram in diagnosing perioperative infarction. The frequent presence of CPK-MB in postoperative patients without other evidence of infarction suggests that further studies are required to identify all factors responsible for its release

Global reduction of cerebral glucose metabolism in persons with symptomatic as well as asymptomatic lacunar infarction

International Nuclear Information System (INIS)

Takahashi, Wakoh; Takagi, Shigeharu; Shinohara, Yukito; Ide, Michiru; Shohtsu, Akira

2000-01-01

To clarify the hemodynamic changes in lacunar infarction, we evaluated cerebral glucose metabolism by using positron emission tomography with 18 F-fluorodeoxyglucose (FDG-PET) in patients with asymptomatic and symptomatic lacunar infarction and in persons without cerebral infarction on MRI. Subjects in this study were 27 patients with symptomatic lacunar infarction (SCI group), 73 subjects with asymptomatic lacunar infarction (ACI group), and 134 persons without infarction (NC group). CMRgI in the ACI group was significantly lower than that in the NC group in the cerebral cortex (P<0.05) and thalamus (P<0.05). CMRgI in the SCI group was significantly reduced from that in the NC group in the cerebral cortex (P<0.005), basal ganglia (P<0.001), thalamus (P<0.05) and white matter (P<0.005). The reduction in CMRgI in the SCI group was more severe than that in the ACI group in basal ganglia (P<0.05) and thalamus (P<0.05). Our results indicated that glucose metabolism in patients with asymptomatic lacunar infarction is reduced throughout the whole brain as compared with non-infarcted elderly persons. Follow-up and treatment of risk factors if present, may be necessary in such patients. (author)

Transplanted Dental Pulp Stem Cells Migrate to Injured Area and Express Neural Markers in a Rat Model of Cerebral Ischemia.

Science.gov (United States)

Zhang, Xuemei; Zhou, Yinglian; Li, Hulun; Wang, Rui; Yang, Dan; Li, Bing; Cao, Xiaofang; Fu, Jin

2018-01-01

Ischemic stroke is a major cause of disability and mortality worldwide, while effective restorative treatments are limited at present. Stem cell transplantation holds therapeutic potential for ischemic vascular diseases and may provide an opportunity for neural regeneration. Dental pulp stem cells (DPSCs) origin from neural crest and have neuro-ectodermal features including proliferation and multilineage differentiation potentials. The rat model of middle cerebral artery occlusion (MCAO) was used to evaluate whether intravenous administration of DPSCs can reduce infarct size and to estimate the migration and trans-differentiation into neuron-like cells in focal cerebral ischemia models. Brain tissues were collected at 4 weeks following cell transplantation and analyzed with immunofluorescence, immunohistochemistry and real-time polymerase chain reaction (RT-PCR) methods. Intravenously administration of rat-derived DPSCs were found to migrate into the boundary of ischemic areas and expressed neural specific markers, reducing infarct volume and cerebral edema. These results suggest that DPSCs treatment may serve as a potential therapy for clinical stroke patients in the future. © 2018 The Author(s). Published by S. Karger AG, Basel.

Classification of myocardial infarction

DEFF Research Database (Denmark)

Saaby, Lotte; Poulsen, Tina Svenstrup; Hosbond, Susanne Elisabeth

2013-01-01

The classification of myocardial infarction into 5 types was introduced in 2007 as an important component of the universal definition. In contrast to the plaque rupture-related type 1 myocardial infarction, type 2 myocardial infarction is considered to be caused by an imbalance between demand...

Contribution of contractile state of the non-infarcted area to global ventricular performance after acute myocardial infarction

International Nuclear Information System (INIS)

Nishimura, Tsunehiko; Yasuda, Tsunehiro; Gold, H.K.; Leinbach, R.C.; Boucher, C.A.; McKusick, K.A.; Strauss, H.W.

1986-01-01

To evaluate the regional contractile state of the non-infarcted zone and to determine the contribution of this area to left ventricular (LV) performance, 112 patients (42 anterior and 70 inferior infarction) with their first acute myocardial infarction were investigated by radionuclide ventriculography at admission and 10 days after admission. Wall motion at the non-infarcted area was defined as hyperkinetic, normal, or hypokinetic, if radial chord shortening had above normal, normal, or below normal values, respectively, by quantitative wall motion analysis. Hyperkinetic, normal, and hypokinetic wall motion of the non-infarcted area were observed in three (7 %), 12 (29 %), and 27 (64 %) patients in anterior infarction and 14 (20 %), 28 (40 %), and 28 (40 %) in inferior infarction, respectively. In the patients with hypokinetic wall motion at the non-infarcted area, the infarct involved more than 30 % of the left ventricle manifesting akinetic contractile segment (ACS), radial chord shortening in the infarcted area was severely depressed, and the incidence of multi-vessel involvement was higher compared with those with hyperkinetic or normal wall motion. In serial measurements, radial chord shortening in the infarcted and non-infarcted area, percent ACS, left ventricular ejection fraction, and left ventricular end-diastolic volume index did not change significantly from acute to follow-up study in any group. In conclusion, our data indicated that the non-infarcted area following acute infarction had various contractile states and these conditions were determined primarily by the severity and extent of infarct and underlying coronary artery disease. Furthermore, the contractile state of the non-infarcted area has a supplemental role in determination of LV function following acute infarction. (author)

Myocardial infarction

International Nuclear Information System (INIS)

Ando, Jyoji; Yasuda, Hisakazu; Miyamoto, Atsushi; Kobayashi, Tsuyoshi

1980-01-01

sup(99m)Tc-pyrophosphate (PYP) scintigraphy and 201 Tl myocardial scintigraphy were utilized for the diagnoses of the presence, the region, and the extent of myocardial infarction. Exercise 201 Tl myocardial scintigrams and exercise radionuclide ventriculography were utilized for diagnosis of coronary artery lesions in angina pectoris. Radionuclide ventriculography was used to investigate effects of coronary artery lesions on cardiac function and hemodynamics. In order to select adequate treatments for myocardial infarction and estimate the prognosis, it was necessary to detect the presence, the region, and the extent of acute myocardial infarction and to investigate effects of partial infarction on hemodynamics by using radionuclide imaging. Exercise myocardial scintigraphy could be carried out noninvasively and repeatedly for diagnosis of coronal artery disease. Therefore, this method could be applied widely. It was possible to use this method as a screening test of coronary artery diseases for the diagnoses of asymptomatic patients who showed ST changes in ECG, the patients with cardiac neurosis and the patency after a reconstructive surgery of coronary artery. (Tsunoda, M.)

Effect of thrombolytic therapy on exercise response during early recovery from acute myocardial infarction

DEFF Research Database (Denmark)

Svendsen, J H; Madsen, J K; Saunamäki, K I

1992-01-01

Several studies have shown that infarct size is reduced following thrombolytic treatment in patients with acute myocardial infarction. Exercise test variables, such as an impaired heart rate response during exercise, are known to be related to left ventricular function and patient prognosis follo...

Overestimation of myocardial infarct size on two-dimensional echocardiograms due to remodelling of the infarct zone.

Science.gov (United States)

Johnston, B J; Blinston, G E; Jugdutt, B I

1994-01-01

To assess the effect of early regional diastolic shape distortion or bulging of infarct zones due to infarct expansion on estimates of regional left ventricular dysfunction and infarct size by two-dimensional echocardiographic imaging. Quantitative two-dimensional echocardiograms from patients with a first Q wave myocardial infarction and creatine kinase infarct size data, and normal subjects, were subjected to detailed analysis of regional left ventricular dysfunction and shape distortion in short-axis images by established methods. Regional left ventricular asynergy (akinesis and dyskinesis) and shape distortion indices (eg, peak [Pk]/radius [ri]) were measured on endocardial diastolic outlines of short-axis images in 43 postinfarction patients (28 anterior and 15 inferior, 5.9 h after onset) and 11 normal subjects (controls). In the infarction group, endocardial surface area of asynergy was calculated by three-dimensional reconstruction of the images and infarct size from serial creatine kinase blood levels. Diastolic bulging of asynergic zones was found in all infarction patients. The regional shape distortion indices characterizing the area between the 'actual' bulging asynergic segment and the derived 'ideal' circular segment (excluding the bulge) on indexed sections were greater in infarct than control groups (Pk/ri 0.31 versus 0, P 0.001). Importantly, the degree of distortion correlated with overestimation of asynergy (r = 0.89, P < 0.001), and the relation between infarct size and total 'ideal' asynergy showed a leftward shift from that with 'actual' asynergy. Early regional diastolic bulging of the infarct zone results in overestimation of regional ventricular dysfunction, especially in patients with anterior infarction. This effect should be considered when assessing effects of therapy on infarct size, remodelling and dysfunction using tomographical imaging.

The effect of ibuprofen on accumulation of indium-111-labeled platelets and leukocytes in experimental myocardial infarction

International Nuclear Information System (INIS)

Romson, J.L.; Hook, B.G.; Rigot, V.H.; Schark, M.A.; Swanson, D.P.; Lucchesi, B.R.

1982-01-01

To assess the ability of ibuprofen to influence the extent of platelet aggregation and leukocyte infiltration during acute myocardial infarction, autologous indium-111 ( 111 In)-labeled platelets or leukocytes were injected before 60 minutes of left circumflex coronary artery (LCx) occlusion, followed by 24 hours of reperfusion in the canine heart. Myocardial infarct size, as a percent of the area at risk, was reduced in the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30 minutes before LCx occulsion) by 40%, from 48 +/- 4% in control animals to 29 +/- 4% in ibuprofen-treated dogs (p=0.005). Quantification of the platelet-associated 111 In radioactivity in irreversibly injured myocardium indicated that ibuprofen did not alter the accumulation of platelets in infarcted myocardium. In contrast, leukocyte accumulation in infarcted tissue was reduced significantly. In tissue samples with 0.41-0.60 gram infarct, the infarcted/normal ratio of leukocyte radioactivity was 12 +/- 2 in control dogs and 4 +/- 1 in ibuprofen-treated dogs, which represents a 67% reduction in leukocyte accumulation in ibuprofen-treated compared with control dogs. Similar reductions were found in other gram-infarct-weight categories. Although both platelets and leukocytes acumulate in infarcted canine myocardium, ibuprofen may exert its beneficial effect on ischemic myocardium by suppressing the inflammatory response associated with myocardial ischemia and infarction

The effect of ibuprofen on accumulation of 111In-labeled platelets and leukocytes in experimental myocardial infarction

International Nuclear Information System (INIS)

Romson, J.L.; Hook, B.G.; Rigot, V.H.; Schork, M.A.; Swanson, D.P.; Lucchesi, B.R.

1982-01-01

To assess the ability of ibuprofen to influence the extent of platelet aggregation and leukocyte infiltration during acute myocardial infarction, autologous indium-111 ( 111 In)-labeled platelets or leukocytes were injected before 60 minutes of left circumflex coronary artery (LCx) occlusion, followed by 24 hours of reperfusion in the canine heart. Myocardial infarct size, as a percent of the area at risk, was reduced in the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30 minutes before LCx occlusion) by 40%, from 48 +/- 4% in control animals to 29 +/- 4% in ibuprofen-treated dogs (p . 0.005). Quantification of the platelet-associated 111 In radioactivity in irreversibly injured myocardium indicated that ibuprofen did not alter the accumulation of platelets in infarcted myocardium. In contrast, leukocyte accumulation in infarcted tissue was reduced significantly. In tissue samples with 0.41-0.60 gram infarct, the infarcted/normal ratio of leukocyte radioactivity was 12 +/- 2 in control dogs and 4 +/- 1 in ibuprofen-treated dogs, which represents a 67% reduction in leukocyte accumulation in ibuprofen-treated compared with control dogs. Similar reductions were found in other gram-infarct-weight categories. Although both platelets and leukocytes accumulate in infarcted canine myocardium, ibuprofen may exert its beneficial effect on ischemic myocardium by suppressing the inflammatory response associated with myocardial ischemia and infarction

Growth factor-induced mobilization of cardiac progenitor cells reduces the risk of arrhythmias, in a rat model of chronic myocardial infarction.

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Leonardo Bocchi

Full Text Available Heart repair by stem cell treatment may involve life-threatening arrhythmias. Cardiac progenitor cells (CPCs appear best suited for reconstituting lost myocardium without posing arrhythmic risks, being commissioned towards cardiac phenotype. In this study we tested the hypothesis that mobilization of CPCs through locally delivered Hepatocyte Growth Factor and Insulin-Like Growth Factor-1 to heal chronic myocardial infarction (MI, lowers the proneness to arrhythmias. We used 133 adult male Wistar rats either with one-month old MI and treated with growth factors (GFs, n = 60 or vehicle (V, n = 55, or sham operated (n = 18. In selected groups of animals, prior to and two weeks after GF/V delivery, we evaluated stress-induced ventricular arrhythmias by telemetry-ECG, cardiac mechanics by echocardiography, and ventricular excitability, conduction velocity and refractoriness by epicardial multiple-lead recording. Invasive hemodynamic measurements were performed before sacrifice and eventually the hearts were subjected to anatomical, morphometric, immunohistochemical, and molecular biology analyses. When compared with untreated MI, GFs decreased stress-induced arrhythmias and concurrently prolonged the effective refractory period (ERP without affecting neither the duration of ventricular repolarization, as suggested by measurements of QTc interval and mRNA levels for K-channel α-subunits Kv4.2 and Kv4.3, nor the dispersion of refractoriness. Further, markers of cardiomyocyte reactive hypertrophy, including mRNA levels for K-channel α-subunit Kv1.4 and β-subunit KChIP2, interstitial fibrosis and negative structural remodeling were significantly reduced in peri-infarcted/remote ventricular myocardium. Finally, analyses of BrdU incorporation and distribution of connexin43 and N-cadherin indicated that cytokines generated new vessels and electromechanically-connected myocytes and abolished the correlation of infarct size with deterioration

Scintigraphic demonstration of acute myocardial infarcts

International Nuclear Information System (INIS)

Holman, B.L.; Lesch, M.

1976-01-01

The feasibility of acute infarct scintigraphy for the clinical evaluation of patients with known or suspected acute myocardial infarction is established. Further development of this methodologic approach may result in even better agents for the visualization of infarcts. Radiotracers with high affinity for the infarct, rapid blood clearance, and low concentrations in surrounding organs, such as liver and bone, would be more suitable than available radiopharmaceuticals for acute myocardial infarct scintigraphy. Ultimately, labeling these tracers and ultra-short-lived radionuclides will enable rapid sequential imaging to assess changes in the extent of infarction and to determine the efficacy of therapies aimed at limiting infarct size

MR imaging of neonatal cerebral infarction

International Nuclear Information System (INIS)

McArdle, C.B.; Mehta, S.D.; Kulkarni, M.V.; Keeney, S.A.; Hayden, C.K.; Adcock, E.W. III.

1987-01-01

Twenty-six neonatal infarcts were imaged with 0.6 T and 1.5-T magnets and correlated with US and/or CT. Periventricular leukomalacia (PVL) was seen in six cases: lobar infarction, ten cases; global infarction, six cases; and basal ganglia infarction, four cases. MR imaging was superior to US and CT in detecting hemorrhagic PVL and basal ganglia infarcts. MR demonstrates lobar infarcts better than US and CT because of a wider field of view, specificty, and improved gray and white matter differentiation. US underestimates the extent of brain destruction in global infarcts. These results indicate that MR is the single best imaging modality for detecting ischemic brain injury

Limitation of myocardial infarct size and preservation of left ventricular function by early administration of APSAC in myocardial infarction.

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Bassand, J P; Machecourt, J; Cassagnes, J; Lusson, J R; Borel, E; Schiele, F

1989-07-05

In cases of acute myocardial infarction (MI), it has been shown that preserving left ventricular function and limiting infarct size with early reperfusion of the occluded artery by means of a thrombolytic agent could eventually result in a reduced mortality rate. The aim of the APSIM study (anisoylated plasminogen streptokinase activator complex [APSAC] dans l'infarctus du Myocarde) was to demonstrate that early administration of APSAC in patients with recent acute MI could limit the infarct size and preserve left ventricular systolic function. In all, 231 patients with a first acute MI were randomly allocated to either APSAC (30 U over 5 minutes) or to conventional heparin therapy (5,000 IU in bolus injection) within 5 hours of the onset of symptoms. Of these patients, 112 received APSAC and 119 received heparin within a mean period of 188 +/- 62 minutes after the onset of symptoms. The patency rate of the infarct-related artery was 77% in the APSAC group and 36% in the heparin group (p less than 0.001). Left ventricular ejection fraction determined from contrast angiography was significantly higher in the APSAC than in the heparin group. This was true for the entire population (0.53 +/- 0.13 vs 0.47 +/- 0.13, p = 0.002) as well as for the subgroups of anterior and inferior wall infarctions (0.47 +/- 0.13 vs 0.4 +/- 0.16, p = 0.004 and 0.56 +/- 0.11 vs 0.51 +/- 0.09, p = 0.02). At 3 weeks, the difference remained significant for patients with anterior MI.(ABSTRACT TRUNCATED AT 250 WORDS)

FFR-guided multivessel stenting reduces urgent revascularization compared with infarct-related artery only stenting in ST-elevation myocardial infarction: A meta-analysis of randomized controlled trials.

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Gupta, Ankur; Bajaj, Navkaranbir S; Arora, Pankaj; Arora, Garima; Qamar, Arman; Bhatt, Deepak L

2018-02-01

Randomized controlled trials (RCTs) have shown fractional flow reserve-guided (FFR) multivessel stenting to be superior to infarct-related artery (IRA) only stenting in patients with ST-elevation myocardial infarction (STEMI) and multivessel disease. This effect was mainly driven by a reduction in overall repeat revascularization. However, the ability to assess the effect of this strategy on urgent revascularization or reinfarction was underpowered in individual trials. We searched Pubmed, EMBASE, Cochrane CENTRAL, and Web of Science for RCTs of FFR-guided multivessel stenting versus IRA-only stenting in STEMI with multivessel disease. The outcomes of interest were death, reinfarction, urgent, and non-urgent repeat revascularization. Risk ratios (RR) were pooled using the DerSimonian and Laird random-effects model. After review of 786 citations, 2 RCTs were included. The pooled results demonstrated a significant reduction in the composite of death, reinfarction, or revascularization in the FFR-guided multivessel stenting group versus IRA-only stenting group (RR [95%, Confidence Interval]: 0.49 [0.33-0.72], p<0.001). This risk reduction was driven mainly by a reduction in repeat revascularization, both urgent (0.41 [0.24-0.71], p=0.002) and non-urgent revascularization (0.31 [0.19-0.50], p<0.001). Pooled RR for reinfarction was lower in the FFR-guided strategy, but was not statistically significant (0.71[0.39-1.31], p=0.28). This systematic review and meta-analysis suggests that a strategy of FFR-guided multivessel stenting in STEMI patients reduces not only overall repeat revascularization but also urgent revascularization. The effect on reinfarction needs to be evaluated in larger trials. Copyright © 2017 Elsevier Ireland Ltd. All rights reserved.

Numerical simulation model of hyperacute/acute stage white matter infarction.

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Sakai, Koji; Yamada, Kei; Oouchi, Hiroyuki; Nishimura, Tsunehiko

2008-01-01

Although previous studies have revealed the mechanisms of changes in diffusivity (apparent diffusion coefficient [ADC]) in acute brain infarction, changes in diffusion anisotropy (fractional anisotropy [FA]) in white matter have not been examined. We hypothesized that membrane permeability as well as axonal swelling play important roles, and we therefore constructed a simulation model using random walk simulation to replicate the diffusion of water molecules. We implemented a numerical diffusion simulation model of normal and infarcted human brains using C++ language. We constructed this 2-pool model using simple tubes aligned in a single direction. Random walk simulation diffused water. Axon diameters and membrane permeability were then altered in step-wise fashion. To estimate the effects of axonal swelling, axon diameters were changed from 6 to 10 microm. Membrane permeability was altered from 0% to 40%. Finally, both elements were combined to explain increasing FA in the hyperacute stage of white matter infarction. The simulation demonstrated that simple water shift into the intracellular space reduces ADC and increases FA, but not to the extent expected from actual human cases (ADC approximately 50%; FA approximately +20%). Similarly, membrane permeability alone was insufficient to explain this phenomenon. However, a combination of both factors successfully replicated changes in diffusivity indices. Both axonal swelling and reduced membrane permeability appear important in explaining changes in ADC and FA based on eigenvalues in hyperacute-stage white matter infarction.

The role of infarct transmural extent in infarct extension: A computational study.

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Leong, Chin-Neng; Lim, Einly; Andriyana, Andri; Al Abed, Amr; Lovell, Nigel Hamilton; Hayward, Christopher; Hamilton-Craig, Christian; Dokos, Socrates

2017-02-01

Infarct extension, a process involving progressive extension of the infarct zone (IZ) into the normally perfused border zone (BZ), leads to continuous degradation of the myocardial function and adverse remodelling. Despite carrying a high risk of mortality, detailed understanding of the mechanisms leading to BZ hypoxia and infarct extension remains unexplored. In the present study, we developed a 3D truncated ellipsoidal left ventricular model incorporating realistic electromechanical properties and fibre orientation to examine the mechanical interaction among the remote, infarct and BZs in the presence of varying infarct transmural extent (TME). Localized highly abnormal systolic fibre stress was observed at the BZ, owing to the simultaneous presence of moderately increased stiffness and fibre strain at this region, caused by the mechanical tethering effect imposed by the overstretched IZ. Our simulations also demonstrated the greatest tethering effect and stress in BZ regions with fibre direction tangential to the BZ-remote zone boundary. This can be explained by the lower stiffness in the cross-fibre direction, which gave rise to a greater stretching of the IZ in this direction. The average fibre strain of the IZ, as well as the maximum stress in the sub-endocardial layer, increased steeply from 10% to 50% infarct TME, and slower thereafter. Based on our stress-strain loop analysis, we found impairment in the myocardial energy efficiency and elevated energy expenditure with increasing infarct TME, which we believe to place the BZ at further risk of hypoxia. Copyright © 2016 John Wiley & Sons, Ltd. Copyright © 2016 John Wiley & Sons, Ltd.

Effect of myocardial infarction on the function and metabolism of the non-infarcted muscle

International Nuclear Information System (INIS)

Hansen, C.A.

1985-01-01

Rat hearts were infarcted in vivo by ligation of the left ventricular coronary artery. After one or three weeks, the hearts were isolated and perfused in vitro. Despite the onset of hypertrophy, ventricular function was more depressed in the one- and three-week infarcted hearts than in acutely ligated hearts. These data suggested that the depressed mechanical function was due not only to the loss of viable tissue, but also to alterations occurring in the non-infarcted tissue. The inotropic response to extracellular calcium was depressed in infarcted hearts, such that the mechanical performance of the infarcted heart was likely to be limited by the availability of extracellular calcium under physiological conditions. No limitation in energy production was found as indicated by the maintenance of ATP levels, the creatine phosphate/creatine ratio and normal lactate concentrations in the infarcted hearts. Comparison of the rates of substrate oxidation with MVO 2 revealed that, in both the sham and infarcted hearts, substrate oxidation, as estimated by 14 CO 2 production, could not account for the observed MVO 2 . It was found that the rate of 14 CO 2 production from exogenous labeled palmitate underestimated the actual rate of fatty acid oxidation. This resulted from incomplete equilibration of added [ 14 C]-palmitate with the fatty acyl moieties present in acyl carnitine. However, the rate of 14 CO 2 production from exogenous palmitate was lower in the infarcted than sham hearts

Neural Mechanisms and Delayed Gastric Emptying of Liquid Induced Through Acute Myocardial Infarction in Rats

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Nunez, Wilson Ranu Ramirez; Ozaki, Michiko Regina; Vinagre, Adriana Mendes; Collares, Edgard Ferro; Almeida, Eros Antonio de, E-mail: erosaa@cardiol.br [Universidade Estadual de Campinas, Campinas, SP (Brazil)

2015-02-15

In pathological situations, such as acute myocardial infarction, disorders of motility of the proximal gut can trigger symptoms like nausea and vomiting. Acute myocardial infarction delays gastric emptying (GE) of liquid in rats. Investigate the involvement of the vagus nerve, α 1-adrenoceptors, central nervous system GABA{sub B} receptors and also participation of paraventricular nucleus (PVN) of the hypothalamus in GE and gastric compliance (GC) in infarcted rats. Wistar rats, N = 8-15 in each group, were divided as INF group and sham (SH) group and subdivided. The infarction was performed through ligation of the left anterior descending coronary artery. GC was estimated with pressure-volume curves. Vagotomy was performed by sectioning the dorsal and ventral branches. To verify the action of GABA{sub B} receptors, baclofen was injected via icv (intracerebroventricular). Intravenous prazosin was used to produce chemical sympathectomy. The lesion in the PVN of the hypothalamus was performed using a 1mA/10s electrical current and GE was determined by measuring the percentage of gastric retention (% GR) of a saline meal. No significant differences were observed regarding GC between groups; vagotomy significantly reduced % GR in INF group; icv treatment with baclofen significantly reduced %GR. GABA{sub B} receptors were not conclusively involved in delaying GE; intravenous treatment with prazosin significantly reduced GR% in INF group. PVN lesion abolished the effect of myocardial infarction on GE. Gastric emptying of liquids induced through acute myocardial infarction in rats showed the involvement of the vagus nerve, alpha1- adrenergic receptors and PVN.

Neural Mechanisms and Delayed Gastric Emptying of Liquid Induced Through Acute Myocardial Infarction in Rats

International Nuclear Information System (INIS)

Nunez, Wilson Ranu Ramirez; Ozaki, Michiko Regina; Vinagre, Adriana Mendes; Collares, Edgard Ferro; Almeida, Eros Antonio de

2015-01-01

In pathological situations, such as acute myocardial infarction, disorders of motility of the proximal gut can trigger symptoms like nausea and vomiting. Acute myocardial infarction delays gastric emptying (GE) of liquid in rats. Investigate the involvement of the vagus nerve, α 1-adrenoceptors, central nervous system GABA B receptors and also participation of paraventricular nucleus (PVN) of the hypothalamus in GE and gastric compliance (GC) in infarcted rats. Wistar rats, N = 8-15 in each group, were divided as INF group and sham (SH) group and subdivided. The infarction was performed through ligation of the left anterior descending coronary artery. GC was estimated with pressure-volume curves. Vagotomy was performed by sectioning the dorsal and ventral branches. To verify the action of GABA B receptors, baclofen was injected via icv (intracerebroventricular). Intravenous prazosin was used to produce chemical sympathectomy. The lesion in the PVN of the hypothalamus was performed using a 1mA/10s electrical current and GE was determined by measuring the percentage of gastric retention (% GR) of a saline meal. No significant differences were observed regarding GC between groups; vagotomy significantly reduced % GR in INF group; icv treatment with baclofen significantly reduced %GR. GABA B receptors were not conclusively involved in delaying GE; intravenous treatment with prazosin significantly reduced GR% in INF group. PVN lesion abolished the effect of myocardial infarction on GE. Gastric emptying of liquids induced through acute myocardial infarction in rats showed the involvement of the vagus nerve, alpha1- adrenergic receptors and PVN

Neural Mechanisms and Delayed Gastric Emptying of Liquid Induced Through Acute Myocardial Infarction in Rats

Directory of Open Access Journals (Sweden)

Wilson Ranu Ramirez Nunez

2015-02-01

Full Text Available Background: In pathological situations, such as acute myocardial infarction, disorders of motility of the proximal gut can trigger symptoms like nausea and vomiting. Acute myocardial infarction delays gastric emptying (GE of liquid in rats. Objective: Investigate the involvement of the vagus nerve, α 1-adrenoceptors, central nervous system GABAB receptors and also participation of paraventricular nucleus (PVN of the hypothalamus in GE and gastric compliance (GC in infarcted rats. Methods: Wistar rats, N = 8-15 in each group, were divided as INF group and sham (SH group and subdivided. The infarction was performed through ligation of the left anterior descending coronary artery. GC was estimated with pressure-volume curves. Vagotomy was performed by sectioning the dorsal and ventral branches. To verify the action of GABAB receptors, baclofen was injected via icv (intracerebroventricular. Intravenous prazosin was used to produce chemical sympathectomy. The lesion in the PVN of the hypothalamus was performed using a 1mA/10s electrical current and GE was determined by measuring the percentage of gastric retention (% GR of a saline meal. Results: No significant differences were observed regarding GC between groups; vagotomy significantly reduced % GR in INF group; icv treatment with baclofen significantly reduced %GR. GABAB receptors were not conclusively involved in delaying GE; intravenous treatment with prazosin significantly reduced GR% in INF group. PVN lesion abolished the effect of myocardial infarction on GE. Conclusion: Gastric emptying of liquids induced through acute myocardial infarction in rats showed the involvement of the vagus nerve, alpha1- adrenergic receptors and PVN.

Plasma HDL cholesterol and risk of myocardial infarction

DEFF Research Database (Denmark)

Voight, Benjamin F; Peloso, Gina M; Orho-Melander, Marju

2012-01-01

High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease processes...

Predictors of fatal outcome in acute myocardial infarction

International Nuclear Information System (INIS)

Qureshi, O.; Mughal, M.M.

2008-01-01

Myocardial infarction is one of the most common life threatening diagnoses in emergency hospital admissions. Most of the complications occur during the first few hours while the patients are likely to be in the hospital. Although the mortality rate after admission for myocardial infarction has declined significantly over the last two decades but it still remains high. Survival is markedly influenced by age of the patient, presence of different risk factors and complications that patients develop after myocardial infarction. We conducted a study at Armed Forces Institute of Cardiology/National Institute of Heart Diseases (AFIC/NIHD) to document the predictors of mortality in patients with acute myocardial infarction. Patients with first acute myocardial infarction admitted to the hospital from Feb. 2007 to June 2007 were included in the study. It was a descriptive case series study and data was collected on a pre-designed proforma with convenient sampling technique. Patients were assessed clinically with special emphasis on history of typical chest pain and physical examination. Relevant investigations were carried out to establish the diagnosis. Two hundred and fifty cases were assessed. Mean age was 57.94+-14.00 years. Males were 74.4% and Females were 25.6%. Overall in-hospital mortality was 9.2%. Females had a higher mortality (14.06%) as compared to males (7.52%). Mortality was also related with age of the patient and Diabetes Mellitus. Other features adversely affecting the in-hospital mortality included higher Killip class, anterior wall myocardial infarction and higher peak Creatine Kinase (CK) levels. Mortality was also higher in patients who did not receive thrombolytic therapy for different reasons. Patients with certain risk factors are more prone to develop complications and have a higher mortality rate. Identification of some of these risk factors and timely management of complications may reduce mortality. (author)

Mortality rate in type 2 myocardial infarction

DEFF Research Database (Denmark)

Saaby, Lotte; Poulsen, Tina Svenstrup; Diederichsen, Axel Cosmus Pyndt

2014-01-01

myocardial infarction, hypercholesterolemia, high p-creatinine, and diabetes mellitus. The multivariable-adjusted hazard ratio for type 2 myocardial infarction was 2.0 (95% confidence interval, 1.3-3.0). With shock as the only exception, mortality was independent of the triggering conditions leading to type....../119) in those with type 2 myocardial infarction and 26% (92/360) in those with type 1 myocardial infarction (P high age, prior myocardial infarction, type 2...... 2 myocardial infarction. CONCLUSIONS: Mortality in patients with type 2 myocardial infarction is high, reaching approximately 50% after 2 years. Further descriptive and survival studies are needed to improve the scientific evidence on which treatment of type 2 myocardial infarction is based....

Mice Lacking the β2 Adrenergic Receptor Have a Unique Genetic Profile before and after Focal Brain Ischaemia

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Robin E White

2012-08-01

Full Text Available The role of the β2AR (β2 adrenergic receptor after stroke is unclear as pharmacological manipulations of the β2AR have produced contradictory results. We previously showed that mice deficient in the β2AR (β2KO had smaller infarcts compared with WT (wild-type mice (FVB after MCAO (middle cerebral artery occlusion, a model of stroke. To elucidate mechanisms of this neuroprotection, we evaluated changes in gene expression using microarrays comparing differences before and after MCAO, and differences between genotypes. Genes associated with inflammation and cell deaths were enriched after MCAO in both genotypes, and we identified several genes not previously shown to increase following ischaemia (Ccl9, Gem and Prg4. In addition to networks that were similar between genotypes, one network with a central core of GPCR (G-protein-coupled receptor and including biological functions such as carbohydrate metabolism, small molecule biochemistry and inflammation was identified in FVB mice but not in β2KO mice. Analysis of differences between genotypes revealed 11 genes differentially expressed by genotype both before and after ischaemia. We demonstrate greater Glo1 protein levels and lower Pmaip/Noxa mRNA levels in β2KO mice in both sham and MCAO conditions. As both genes are implicated in NF-κB (nuclear factor κB signalling, we measured p65 activity and TNFα (tumour necrosis factor α levels 24 h after MCAO. MCAO-induced p65 activation and post-ischaemic TNFα production were both greater in FVB compared with β2KO mice. These results suggest that loss of β2AR signaling results in a neuroprotective phenotype in part due to decreased NF-κB signalling, decreased inflammation and decreased apoptotic signalling in the brain.

Antiarrhythmic effect of carvedilol after acute myocardial infarction: results of the Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN) trial

DEFF Research Database (Denmark)

McMurray, John; Køber, Lars; Robertson, Michele

2005-01-01

OBJECTIVES: Whether beta-blockers reduce atrial arrhythmias and, when added to an angiotensin-converting enzyme (ACE) inhibitor, ventricular arrhythmia is unknown. BACKGROUND: Ventricular and atrial arrhythmias are common after acute myocardial infarction (AMI) and are associated with a poor prog...

Migrainous infarction

DEFF Research Database (Denmark)

Laurell, K; Artto, V; Bendtsen, L

2011-01-01

Migrainous infarction (MI), i.e. an ischemic stroke developing during an attack of migraine with aura is rare and the knowledge of its clinical characteristics is limited. Previous case series using the International Classification of Headache Disorders (ICHD) included......Migrainous infarction (MI), i.e. an ischemic stroke developing during an attack of migraine with aura is rare and the knowledge of its clinical characteristics is limited. Previous case series using the International Classification of Headache Disorders (ICHD) included...

[Splenic infarction].

Science.gov (United States)

Cuquerella, J; Ferrer, L; Rivera, P; Tuset, J A; Medina, E; Pamós, S; Ariete, V; Tomé, A; García, V

1996-06-01

A 53-year-old male suffered splenic infarction etiologically related to atrial fibrillation and non-obstructive hypertrophic cardiomyopathy. The main clinical manifestations were a one-month history of epigastric and left upper quadrant pain, with tenderness to palpation in the later zone. Laboratory tests revealed a slight leucocytosis (14.700) with left shift and a marked increase in LDH concentration (945 IU). Abdominal CAT and arteriography established the diagnosis, Echography proved normal. Patient evolution was satisfactory with conservative medical treatment. We conclude that splenic infarction should be considered in all cases of acute or chronic pain in the left hypochondrium. The diagnosis is established by CAT, arteriography and hepatosplenic gammagraphy. Medical management is initially advocated, surgery being reserved for those cases involving complications or in which diagnosis is not clear. Emphasis is placed on the main etiological, clinical, diagnostic and management characteristics of splenic infarction.

Suppressing Receptor-Interacting Protein 140: a New Sight for Salidroside to Treat Cerebral Ischemia.

Science.gov (United States)

Chen, Tong; Ma, Zhanqiang; Zhu, Lingpeng; Jiang, Wenjiao; Wei, Tingting; Zhou, Rui; Luo, Fen; Zhang, Kai; Fu, Qiang; Ma, Chunhua; Yan, Tianhua

2016-11-01

The purpose of the current study was to detect the effect of salidroside (Sal) on cerebral ischemia and explore its potential mechanism. Middle cerebral artery occlusion (MCAO) was performed to investigate the effects of Sal on cerebral ischemia. The rats were randomly divided into five groups: sham group, vehicle group, clopidogrel (7.5 mg/kg) group, Sal (20 mg/kg) group, and Sal (40 mg/kg) group. SH-SY5Y cells were exposed to ischemia-reperfusion (I/R) injury to verify the protective effect of Sal in vitro. We also built the stable receptor-interacting protein 140 (RIP140)-overexpressing SH-SY5Y cells. The results showed that Sal significantly reduces brain infarct size and cerebral edema. Sal could effectively decrease the levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in serum of the MCAO rats and supernatant of I/R-induced SH-SY5Y cells. Immunohistochemical and Western blot results demonstrated that Sal inhibited RIP140-mediated inflammation and apoptosis in the MCAO rats and SH-SY5Y cells. In addition, we further confirmed that RIP140/NF-κB signaling plays a crucial role by evaluating the protein expression in RIP140-overexpressing SH-SY5Y cells. Our findings suggested that Sal could be used as an effective neuroprotective agent for cerebral ischemia due to its significant effect on preventing neuronal cell injury after cerebral ischemia both in vivo and in vitro by the inhibitions of RIP140-mediated inflammation and apoptosis.

Study progress of cardiac MRI technology in assessment of myocardial viability after myocardial infarction

International Nuclear Information System (INIS)

Wang Jing; Zhang Hao

2013-01-01

Acute myocardial infarction (AMI) is one of the most common diseases that cause disability and death around the world. Correctly and effectively assessing the myocardial viability after myocardial infarction can reduce the disabled rate and mortality rate. At present, many methods could be used to assess myocardial viability. The cardiac magnetic resonance imaging (CMR) technology has a lot of advantages compared to other methods. In this paper, we reviewed the research progress of CMR in assessment of myocardial viability after myocardial infarction, and compared CMR with other technologies. (authors)

Thiamet G mediates neuroprotection in experimental stroke by modulating microglia/macrophage polarization and inhibiting NF-κB p65 signaling.

Science.gov (United States)

He, Yating; Ma, Xiaofeng; Li, Daojing; Hao, Junwei

2017-08-01

Inflammatory responses are accountable for secondary injury induced by acute ischemic stroke (AIS). Previous studies indicated that O-GlcNAc modification (O-GlcNAcylation) is involved in the pathology of AIS, and increase of O-GlcNAcylation by glucosamine attenuated the brain damage after ischemia/reperfusion. Inhibition of β-N-acetylglucosaminidase (OGA) with thiamet G (TMG) is an alternative option for accumulating O-GlcNAcylated proteins. In this study, we investigate the neuroprotective effect of TMG in a mouse model of experimental stroke. Our results indicate that TMG administration either before or after middle cerebral artery occlusion (MCAO) surgery dramatically reduced infarct volume compared with that in untreated controls. TMG treatment ameliorated the neurological deficits and improved clinical outcomes in neurobehavioral tests by modulating the expression of pro-inflammatory and anti-inflammatory cytokines. Additionally, TMG administration reduced the number of Iba1 + cells in MCAO mice, decreased expression of the M1 markers, and increased expression of the M2 markers in vivo. In vitro, M1 polarization of BV2 cells was inhibited by TMG treatment. Moreover, TMG decreased the expression of iNOS and COX2 mainly by suppressing NF-κB p65 signaling. These results suggest that TMG exerts a neuroprotective effect and could be useful as an anti-inflammatory agent for ischemic stroke therapy.

Resistance Training After Myocardial Infarction in Rats: Its Role on Cardiac and Autonomic Function

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Camilla Figueiredo Grans

2014-07-01

Full Text Available Background: Although resistance exercise training is part of cardiovascular rehabilitation programs, little is known about its role on the cardiac and autonomic function after myocardial infarction. Objective: To evaluate the effects of resistance exercise training, started early after myocardial infarction, on cardiac function, hemodynamic profile, and autonomic modulation in rats. Methods: Male Wistar rats were divided into four groups: sedentary control, trained control, sedentary infarcted and trained infarcted rats. Each group with n = 9 rats. The animals underwent maximum load test and echocardiography at the beginning and at the end of the resistance exercise training (in an adapted ladder, 40% to 60% of the maximum load test, 3 months, 5 days/week. At the end, hemodynamic, baroreflex sensitivity and autonomic modulation assessments were made. Results: The maximum load test increased in groups trained control (+32% and trained infarcted (+46% in relation to groups sedentary control and sedentary infarcted. Although no change occurred regarding the myocardial infarction size and systolic function, the E/A ratio (-23%, myocardial performance index (-39% and systolic blood pressure (+6% improved with resistance exercise training in group trained infarcted. Concomitantly, the training provided additional benefits in the high frequency bands of the pulse interval (+45%, as well as in the low frequency band of systolic blood pressure (-46% in rats from group trained infarcted in relation to group sedentary infarcted. Conclusion: Resistance exercise training alone may be an important and safe tool in the management of patients after myocardial infarction, considering that it does not lead to significant changes in the ventricular function, reduces the global cardiac stress, and significantly improves the vascular and cardiac autonomic modulation in infarcted rats.

Resistance Training After Myocardial Infarction in Rats: Its Role on Cardiac and Autonomic Function

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Grans, Camilla Figueiredo; Feriani, Daniele Jardim; Abssamra, Marcos Elias Vergilino; Rocha, Leandro Yanase; Carrozzi, Nicolle Martins; Mostarda, Cristiano; Figueroa, Diego Mendrot; Angelis, Kátia De; Irigoyen, Maria Cláudia; Rodrigues, Bruno

2014-01-01

Although resistance exercise training is part of cardiovascular rehabilitation programs, little is known about its role on the cardiac and autonomic function after myocardial infarction. To evaluate the effects of resistance exercise training, started early after myocardial infarction, on cardiac function, hemodynamic profile, and autonomic modulation in rats. Male Wistar rats were divided into four groups: sedentary control, trained control, sedentary infarcted and trained infarcted rats. Each group with n = 9 rats. The animals underwent maximum load test and echocardiography at the beginning and at the end of the resistance exercise training (in an adapted ladder, 40% to 60% of the maximum load test, 3 months, 5 days/week). At the end, hemodynamic, baroreflex sensitivity and autonomic modulation assessments were made. The maximum load test increased in groups trained control (+32%) and trained infarcted (+46%) in relation to groups sedentary control and sedentary infarcted. Although no change occurred regarding the myocardial infarction size and systolic function, the E/A ratio (-23%), myocardial performance index (-39%) and systolic blood pressure (+6%) improved with resistance exercise training in group trained infarcted. Concomitantly, the training provided additional benefits in the high frequency bands of the pulse interval (+45%), as well as in the low frequency band of systolic blood pressure (-46%) in rats from group trained infarcted in relation to group sedentary infarcted. Resistance exercise training alone may be an important and safe tool in the management of patients after myocardial infarction, considering that it does not lead to significant changes in the ventricular function, reduces the global cardiac stress, and significantly improves the vascular and cardiac autonomic modulation in infarcted rats

Resistance Training After Myocardial Infarction in Rats: Its Role on Cardiac and Autonomic Function

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Grans, Camilla Figueiredo; Feriani, Daniele Jardim; Abssamra, Marcos Elias Vergilino; Rocha, Leandro Yanase; Carrozzi, Nicolle Martins [Laboratório do Movimento Humano, Universidade São Judas Tadeu (USJT), São Paulo, SP (Brazil); Mostarda, Cristiano [Departamento de Educação Física, Universidade Federal do Maranhão (UFMA), São Luís, MA (Brazil); Figueroa, Diego Mendrot [Laboratório de Hipertensão Experimental, Instituto do Coração (InCor), Faculdade de Medicina, Universidade de São Paulo (USP), São Paulo, SP (Brazil); Angelis, Kátia De [Laboratório de Fisiologia Translacional, Universidade Nove de Julho (Uninove), São Paulo, SP (Brazil); Irigoyen, Maria Cláudia [Laboratório de Hipertensão Experimental, Instituto do Coração (InCor), Faculdade de Medicina, Universidade de São Paulo (USP), São Paulo, SP (Brazil); Rodrigues, Bruno, E-mail: bruno.rodrigues@incor.usp.br [Laboratório do Movimento Humano, Universidade São Judas Tadeu (USJT), São Paulo, SP (Brazil)

2014-07-15

Although resistance exercise training is part of cardiovascular rehabilitation programs, little is known about its role on the cardiac and autonomic function after myocardial infarction. To evaluate the effects of resistance exercise training, started early after myocardial infarction, on cardiac function, hemodynamic profile, and autonomic modulation in rats. Male Wistar rats were divided into four groups: sedentary control, trained control, sedentary infarcted and trained infarcted rats. Each group with n = 9 rats. The animals underwent maximum load test and echocardiography at the beginning and at the end of the resistance exercise training (in an adapted ladder, 40% to 60% of the maximum load test, 3 months, 5 days/week). At the end, hemodynamic, baroreflex sensitivity and autonomic modulation assessments were made. The maximum load test increased in groups trained control (+32%) and trained infarcted (+46%) in relation to groups sedentary control and sedentary infarcted. Although no change occurred regarding the myocardial infarction size and systolic function, the E/A ratio (-23%), myocardial performance index (-39%) and systolic blood pressure (+6%) improved with resistance exercise training in group trained infarcted. Concomitantly, the training provided additional benefits in the high frequency bands of the pulse interval (+45%), as well as in the low frequency band of systolic blood pressure (-46%) in rats from group trained infarcted in relation to group sedentary infarcted. Resistance exercise training alone may be an important and safe tool in the management of patients after myocardial infarction, considering that it does not lead to significant changes in the ventricular function, reduces the global cardiac stress, and significantly improves the vascular and cardiac autonomic modulation in infarcted rats.

Resistance Training After Myocardial Infarction in Rats: Its Role on Cardiac and Autonomic Function

Science.gov (United States)

Grans, Camilla Figueiredo; Feriani, Daniele Jardim; Abssamra, Marcos Elias Vergilino; Rocha, Leandro Yanase; Carrozzi, Nicolle Martins; Mostarda, Cristiano; Figueroa, Diego Mendrot; Angelis, Kátia De; Irigoyen, Maria Cláudia; Rodrigues, Bruno

2014-01-01

Background Although resistance exercise training is part of cardiovascular rehabilitation programs, little is known about its role on the cardiac and autonomic function after myocardial infarction. Objective To evaluate the effects of resistance exercise training, started early after myocardial infarction, on cardiac function, hemodynamic profile, and autonomic modulation in rats. Methods Male Wistar rats were divided into four groups: sedentary control, trained control, sedentary infarcted and trained infarcted rats. Each group with n = 9 rats. The animals underwent maximum load test and echocardiography at the beginning and at the end of the resistance exercise training (in an adapted ladder, 40% to 60% of the maximum load test, 3 months, 5 days/week). At the end, hemodynamic, baroreflex sensitivity and autonomic modulation assessments were made. Results The maximum load test increased in groups trained control (+32%) and trained infarcted (+46%) in relation to groups sedentary control and sedentary infarcted. Although no change occurred regarding the myocardial infarction size and systolic function, the E/A ratio (-23%), myocardial performance index (-39%) and systolic blood pressure (+6%) improved with resistance exercise training in group trained infarcted. Concomitantly, the training provided additional benefits in the high frequency bands of the pulse interval (+45%), as well as in the low frequency band of systolic blood pressure (-46%) in rats from group trained infarcted in relation to group sedentary infarcted. Conclusion Resistance exercise training alone may be an important and safe tool in the management of patients after myocardial infarction, considering that it does not lead to significant changes in the ventricular function, reduces the global cardiac stress, and significantly improves the vascular and cardiac autonomic modulation in infarcted rats. PMID:25014059

Zonal frequency analysis of the gyral and sulcal extent of cerebral infarcts. Part III: Middle cerebral artery and watershed infarcts

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Naidich, T.P.; Firestone, M.I.; Blum, J.T.; Abrams, K.J.

2003-01-01

We tested the hypothesis that frequency analysis of the anatomic zones affected by single anterior (A), posterior (P), and middle (M) cerebral artery (CA), multivessel, and watershed infarcts will disclose specific sites (peak zones) most frequently involved by each type, sites most frequently injured by multiple different types (vulnerable zones), and overlapping sites of equal relative frequency for two or more different types of infarct (equal frequency zones). We adopted precise definitions of each vascular territory. CT and MRI studies of 50 MCA, 20 ACA-MCA, three PCA-MCA, and 30 parasagittal watershed infarcts were mapped onto a standard template. Relative infarct frequencies in each zone were analyzed within and across infarct types to identify the centers and peripheries of each, vulnerable zones, and equal frequency zones. These data were then correlated with the prior analysis of 47 ACA, PCA, dual ACA-PCA, and ACA-PCA-MCA infarcts. Zonal frequency data for MCA and watershed infarcts, the sites of peak infarct frequency, the sites of vulnerability to diverse infarcts, and the overlapping sites of equal infarct frequency are tabulated and displayed in standardized format for direct comparison of different infarcts. This method successfully displays the nature, sites, and extent of individual infarct types, illustrates the shifts in zonal frequency and lesion center that attend dual and triple infarcts, and clarifies the relationships among the diverse types of infarct. (orig.)

Abrupt opium discontinuation has no significant triggering effect on acute myocardial infarction.

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Masoomi, Mohammad; Zare, Jahangir; Nasri, Hamidreza; Mirzazadeh, Ali; Sheikhvatan, Mehrdad

2011-04-01

A deleterious effect of withdrawal symptoms due to abrupt discontinuation of opium on the cardiovascular system is one of the recent interesting topics in the cardiovascular field. The current study hypothesized that the withdrawal syndrome due to discontinuing opium might be an important trigger for the appearance of acute myocardial infarction. Eighty-one opium-addicted individuals who were candidates for cardiovascular clinical evaluation and consecutively hospitalized in the coronary care unit (CCU) ward of Shafa Hospital in Kerman between January and July 2009 were included in the study and categorized in the case group, including patients experiencing withdrawal symptoms within 6-12 h after the reduced or discontinued use of opium according to the Diagnostic and Statistical Manual of Mental Disorders-revised IV version (DSM-IV-R) criteria for opium dependence and withdrawal, and the control group, without opium withdrawal symptoms. The appearance of acute myocardial infarction was compared between the two groups using multivariable regression models. Acute myocardial infarction occurred in 50.0% of those with withdrawal symptoms and in 45.1% of patients without evidence of opium withdrawal (P = 0.669). Multivariable analysis showed that opium withdrawal symptoms were not a trigger for acute myocardial infarction adjusting for demographic characteristics, marital status, education level and common coronary artery disease risk profiles [odds ratio (OR) = 0.920, 95% confidence interval (CI) = 0.350-2.419, P = 0.866]. Also, daily dose of opium before reducing or discontinuing use did not predict the appearance of myocardial infarction in the presence of confounder variables (OR = 0.975, 95% CI = 0.832-1.143, P = 0.755). Withdrawal syndrome due to abrupt discontinuation of opium does not have a triggering role for appearance of acute myocardial infarction.

Multimodality imaging of pulmonary infarction

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Bray, T.J.P.; Mortensen, K.H.; Gopalan, D.

2014-01-01

Highlights: • A plethora of pulmonary and systemic disorders, often associated with grave outcomes, may cause pulmonary infarction. • A stereotypical infarct is a peripheral wedge shaped pleurally based opacity but imaging findings can be highly variable. • Multimodality imaging is key to diagnosing the presence, aetiology and complications of pulmonary infarction. • Multimodality imaging of pulmonary infarction together with any ancillary features often guide to early targeted treatment. • CT remains the principal imaging modality with MRI increasingly used alongside nuclear medicine studies and ultrasound. - Abstract: The impact of absent pulmonary arterial and venous flow on the pulmonary parenchyma depends on a host of factors. These include location of the occlusive insult, the speed at which the occlusion develops and the ability of the normal dual arterial supply to compensate through increased bronchial arterial flow. Pulmonary infarction occurs when oxygenation is cut off secondary to sudden occlusion with lack of recruitment of the dual supply arterial system. Thromboembolic disease is the commonest cause of such an insult but a whole range of disease processes intrinsic and extrinsic to the pulmonary arterial and venous lumen may also result in infarcts. Recognition of the presence of infarction can be challenging as imaging manifestations often differ from the classically described wedge shaped defect and a number of weighty causes need consideration. This review highlights aetiologies and imaging appearances of pulmonary infarction, utilising cases to illustrate the essential role of a multimodality imaging approach in order to arrive at the appropriate diagnosis

Multimodality imaging of pulmonary infarction

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Bray, T.J.P., E-mail: timothyjpbray@gmail.com [Department of Radiology, Papworth Hospital NHS Foundation Trust, Ermine Street, Papworth Everard, Cambridge CB23 3RE (United Kingdom); Mortensen, K.H., E-mail: mortensen@doctors.org.uk [Department of Radiology, Papworth Hospital NHS Foundation Trust, Ermine Street, Papworth Everard, Cambridge CB23 3RE (United Kingdom); University Department of Radiology, Addenbrookes Hospital, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Box 318, Cambridge CB2 0QQ (United Kingdom); Gopalan, D., E-mail: deepa.gopalan@btopenworld.com [Department of Radiology, Papworth Hospital NHS Foundation Trust, Ermine Street, Papworth Everard, Cambridge CB23 3RE (United Kingdom)

2014-12-15

Highlights: • A plethora of pulmonary and systemic disorders, often associated with grave outcomes, may cause pulmonary infarction. • A stereotypical infarct is a peripheral wedge shaped pleurally based opacity but imaging findings can be highly variable. • Multimodality imaging is key to diagnosing the presence, aetiology and complications of pulmonary infarction. • Multimodality imaging of pulmonary infarction together with any ancillary features often guide to early targeted treatment. • CT remains the principal imaging modality with MRI increasingly used alongside nuclear medicine studies and ultrasound. - Abstract: The impact of absent pulmonary arterial and venous flow on the pulmonary parenchyma depends on a host of factors. These include location of the occlusive insult, the speed at which the occlusion develops and the ability of the normal dual arterial supply to compensate through increased bronchial arterial flow. Pulmonary infarction occurs when oxygenation is cut off secondary to sudden occlusion with lack of recruitment of the dual supply arterial system. Thromboembolic disease is the commonest cause of such an insult but a whole range of disease processes intrinsic and extrinsic to the pulmonary arterial and venous lumen may also result in infarcts. Recognition of the presence of infarction can be challenging as imaging manifestations often differ from the classically described wedge shaped defect and a number of weighty causes need consideration. This review highlights aetiologies and imaging appearances of pulmonary infarction, utilising cases to illustrate the essential role of a multimodality imaging approach in order to arrive at the appropriate diagnosis.

Computerized tomography of cerebral infarction

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Yamashita, K; Mihara, T; Kobayashi, E; Yamamoto, K; Kusumoto, K [Kagoshima Univ. (Japan). Faculty of Medicine

1978-12-01

In 120 cases of patients with cerebral infarction, the affected areas in the CT images were analyzed with special reference to the site, the size, and the extension. Moreover, on 39 scans of 34 cases examined with 8 weeks after the onset of strokes, the CT images were analyzed from the viewpoint of the presence of a mass effect, edema, contrast enhancement, and the accompanying hemorrhage. From these investigations, the authors have obtained the following results; 1) The greatest incidence of infarcts was in the area supplied by the middle cerebral artery (57% of the cases), and, among those, the area of the lenticulostriate arteries showed the highest incidence (53%). Even in the posterior fossa, infarcts were found in 6% of the cases. These findings are coincident with those in autopsied cases. 2) Putaminal infarcts and infarctions occurring in the area supplied by the calcarine artery seemed to be uniformity of the arcuate pattern. 3) Most of the infarcts in the perfusion area of the anterior cerebral artery and the basal ganglia were found to be small and multifocal; they were thought to correspond with water-shed and/or lacunar infarcts. 4) In approximately 25% of the cases examined within 8 weeks after the onset of strokes, the CT images revealed mass effects which had never been observed after more than 3 weeks. In conclusion, the presence of a mass effect, accompanying hemorrhage, and contrast enhancement detected by CT should lead us to reconsider the conventional management of cerebral infarction.

Does menopausal hormone therapy reduce myocardial infarction risk if initiated early after menopause? A population-based case-control study.

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Carrasquilla, Germán D; Berglund, Anita; Gigante, Bruna; Landgren, Britt-Marie; de Faire, Ulf; Hallqvist, Johan; Leander, Karin

2015-06-01

This study aims to assess whether the timing of menopausal hormone therapy initiation in relation to onset of menopause and hormone therapy duration is associated with myocardial infarction risk. This study was based on the Stockholm Heart Epidemiology Program, a population-based case-control study including 347 postmenopausal women who had experienced a nonfatal myocardial infarction and 499 female control individuals matched for age and residential area. Odds ratios (with 95% CIs) for myocardial infarction were calculated using logistic regression. Early initiation of hormone therapy (within 10 y of onset of menopause or before age 60 y), compared with never use, was associated with an odds ratio of 0.87 (95% CI, 0.58-1.30) after adjustments for lifestyle factors, body mass index, and socioeconomic status. For late initiation of hormone therapy, the corresponding odds ratio was 0.97 (95% CI, 0.53-1.76). For hormone therapy duration of 5 years or more, compared with never use, the adjusted odds ratio was 0.64 (95% CI, 0.35-1.18). For hormone therapy duration of less than 5 years, the odds ratio was 0.97 (95% CI, 0.63-1.48). Neither the timing of hormone therapy initiation nor the duration of therapy is significantly associated with myocardial infarction risk.

Massive cerebellar infarction: a neurosurgical approach

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Salazar Luis Rafael Moscote

2015-12-01

Full Text Available Cerebellar infarction is a challenge for the neurosurgeon. The rapid recognition will crucial to avoid devastating consequences. The massive cerebellar infarction has pseudotumoral behavior, should affect at least one third of the volume of the cerebellum. The irrigation of the cerebellum presents anatomical diversity, favoring the appearance of atypical infarcts. The neurosurgical management is critical for massive cerebellar infarction. We present a review of the literature.

Brief pressure overload of the left ventricle reduces myocardial infarct size via activation of protein kinase C.

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Tang, Chia-Yu; Lai, Chang-Chi; Chiang, Shu-Chiung; Tseng, Kuo-Wei; Huang, Cheng-Hsiung

2015-09-01

We have previously reported that brief pressure overload of the left ventricle reduced myocardial infarct (MI) size. However, the role of protein kinase C (PKC) remains uncertain. In this study, we investigated whether pressure overload reduces MI size by activating PKC. MI was induced by a 40-minute occlusion of the left anterior descending coronary artery and a 3-hour reperfusion in anesthetized Sprague-Dawley rats. MI size was determined using triphenyl tetrazolium chloride staining. Brief pressure overload was achieved by two 10-minute partial snarings of the ascending aorta, raising the systolic left ventricular pressure 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions and 10-minute reperfusions. Dimethyl sulfoxide (vehicle) or calphostin C (0.1 mg/kg, a specific inhibitor of PKC) was administered intravenously as pretreatment. The MI size, expressed as the percentage of the area at risk, was significantly reduced in the pressure overload group and the ischemic preconditioning group (19.0 ± 2.9% and 18.7 ± 3.0% vs. 26.1 ± 2.6% in the control group, where p overload and ischemic preconditioning (25.2 ± 2.4% and 25.0 ± 2.3%, where p overload of the left ventricle reduced MI size. Since calphostin C significantly limited the decrease of MI size, our results suggested that brief pressure overload reduces MI size via activation of PKC. Copyright © 2015. Published by Elsevier Taiwan.

From the Cover: Lifelong Exposure of C57bl/6n Male Mice to Bisphenol A or Bisphenol S Reduces Recovery From a Myocardial Infarction.

Science.gov (United States)

Kasneci, Amanda; Lee, Jun Seong; Yun, Tae Jin; Shang, Jijun; Lampen, Shaun; Gomolin, Tamar; Cheong, Cheolho C; Chalifour, Lorraine E

2017-09-01

Bisphenol A (BPA) leaches from plastics to contaminate foodstuffs. Analogs, such as bisphenol S (BPS), are now used increasingly in manufacturing. Greater BPA exposure has been correlated with exacerbation of cardiovascular disease, including myocardial infarction (MI). To test the hypothesis that bisphenol exposure impairs cardiac healing, we exposed C57bl/6n mice to water containing 25ng/ml BPA or BPS from conception and surgically induced an MI in adult male progeny. Increased early death and cardiac dilation, and reduced cardiac function were found post-MI in BPA- and BPS-exposed mice. Flow cytometry revealed increased monocyte and macrophage infiltration that correlated with increased chemokine C-C motif ligand-2 expression in the infarct. In vitro BPA and BPS addition increased matrix metalloproteinase-9 (MMP) protein and secreted activity in RAW264.7 macrophage cells suggesting that invivo increases in MMP2 and MMP9 in exposed infarcts were myeloid-derived. Bone marrow-derived monocytes isolated from exposed mice had greater expression of pro-inflammatory polarization markers when chemokine stimulated indicating an enhanced susceptibility to develop a pro-inflammatory monocyte population. Chronic BPA exposure of estrogen receptor beta (ERβ) deficient mice did not worsen early death, cardiac structure/function, or expression of myeloid markers after an MI. In contrast, BPS exposure of ERβ-deficient mice resulted in greater death and expression of myeloid markers. We conclude that lifelong exposure to BPA or BPS augmented the monocyte/macrophage inflammatory response and adverse remodeling from an MI thereby reducing the ability to survive and successfully recover, and that the adverse effect of BPA, but not BPS, is downstream of ERβ signaling. © The Author 2017. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Comparison of blood biochemics between acute myocardial infarction models with blood stasis and simple acute myocardial infarction models in rats

International Nuclear Information System (INIS)

Qu Shaochun; Yu Xiaofeng; Wang Jia; Zhou Jinying; Xie Haolin; Sui Dayun

2010-01-01

Objective: To construct the acute myocardial infarction models in rats with blood stasis and study the difference on blood biochemics between the acute myocardial infarction models with blood stasis and the simple acute myocardial infarction models. Methods: Wistar rats were randomly divided into control group, acute blood stasis model group, acute myocardial infarction sham operation group, acute myocardial infarction model group and of acute myocardial infarction model with blood stasis group. The acute myocardial infarction models under the status of the acute blood stasis in rats were set up. The serum malondialdehyde (MDA), nitric oxide (NO), free fatty acid (FFA), tumor necrosis factor-α (TNF-α) levels were detected, the activities of serum superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the levels of prostacycline (PGI2), thromboxane A 2 (TXA 2 ) and endothelin (ET) in plasma were determined. Results: There were not obvious differences in MDA, SOD, GSH-Px and FFA between the acute myocardial infarction models with blood stasis in rats and the simple acute myocardial infarction models (P 2 and NO, and the increase extents of TXA 2 , ET and TNF-α in the acute myocardial infarction models in rats with blood stasis were higher than those in the simple acute myocardial infarction models (P 2 and NO, are significant when the acute myocardial infarction models in rats with blood stasis and the simple acute myocardial infarction models are compared. The results show that it is defective to evaluate pharmacodynamics of traditional Chinese drug with only simple acute myocardial infarction models. (authors)

Cardiac-Restricted IGF-1Ea Overexpression Reduces the Early Accumulation of Inflammatory Myeloid Cells and Mediates Expression of Extracellular Matrix Remodelling Genes after Myocardial Infarction

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Enrique Gallego-Colon

2015-01-01

Full Text Available Strategies to limit damage and improve repair after myocardial infarct remain a major therapeutic goal in cardiology. Our previous studies have shown that constitutive expression of a locally acting insulin-like growth factor-1 Ea (IGF-1Ea propeptide promotes functional restoration after cardiac injury associated with decreased scar formation. In the current study, we investigated the underlying molecular and cellular mechanisms behind the enhanced functional recovery. We observed improved cardiac function in mice overexpressing cardiac-specific IGF-1Ea as early as day 7 after myocardial infarction. Analysis of gene transcription revealed that supplemental IGF-1Ea regulated expression of key metalloproteinases (MMP-2 and MMP-9, their inhibitors (TIMP-1 and TIMP-2, and collagen types (Col 1α1 and Col 1α3 in the first week after injury. Infiltration of inflammatory cells, which direct the remodelling process, was also altered; in particular there was a notable reduction in inflammatory Ly6C+ monocytes at day 3 and an increase in anti-inflammatory CD206+ macrophages at day 7. Taken together, these results indicate that the IGF-1Ea transgene shifts the balance of innate immune cell populations early after infarction, favouring a reduction in inflammatory myeloid cells. This correlates with reduced extracellular matrix remodelling and changes in collagen composition that may confer enhanced scar elasticity and improved cardiac function.

Integrated pharmacokinetics of major bioactive components in MCAO rats after oral administration of Huang-Lian-Jie-Du-Tang.

Science.gov (United States)

Zhu, Huaxu; Qian, Zhilei; Li, Huan; Guo, Liwei; Pan, Linmei; Zhang, Qichun; Tang, Yuping

2012-05-07

Huang-Lian-Jie-Du-Tang (HLJDT, or Oren-gedoku-to in Japanese), an important multi-herb remedy in China and other Asia countries, has been used clinically to treat cerebral ischemia for decades. According to the previous studies we have reported, an HPLC method was developed and validated for determination of berberine, palmatine, baicalin, baicalein and geniposide simultaneously in MCAO rat plasma after administration of HLJDT aqueous extract. A classified integral pharmacokinetic method was put forward after having compared the integrated concentration-time profile with that of single component. An AUC based weighting approach was used for integrated principle. The results indicated the classified integral pharmacokinetic profile of index components from HLJDT could reveal the pharmacokinetic behavior of original components, and was corresponding to the holistic pharmacological effects of anti-ischemia with HLJDT. This study was aimed to explore an approach that could be applied to integrate the pharmacokinetic behavior of different components derived from HLJDT. The integrated pharmacokinetic results also provided more information for further understanding of the clinical cerebrovascular disease in use of HLJDT. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

Is enhanced MRI helpful in brainstem infarction?

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Jeong, Y. M.; Shin, G. H.; Choi, W. S. [Kyung Hee University Hospital, Seoul (Korea, Republic of)

1994-12-15

To determine the role of MR contrast enhancement in evaluating time course of brainstem infarction. MR imaging with IV administration of gadopentetate dimeglumine was retrospectively reviewed in 43 patients with clinically and radiologically documented brainstem infarctions. The pattern of infarction was classified into spotty and patchy. Presence of parenchymal enhancement in infarction was evaluated. By location, there were 34 pontine, 3 midbrain, 6 medullary infarctions. The age of the infarctions ranged from 1 day to 9 months, with 5 patients scanned within 3 days and 10 scanned within 2 weeks of clinical ictus. Abnormalities on T2-weighted images were encountered in every case, with spotty pattern in 14 cases and patchy pattern in 29 cases. Parenchymal contrast enhancement was seen in 9 cases(20%), primarily occurring between days 8 and 20. MR contrast enhancement in brainstem infarction was infrequent that it may not be useful in the estimation of the age of infarction.

Relaxin reduces susceptibility to post-infarct atrial fibrillation in mice due to anti-fibrotic and anti-inflammatory properties.

Science.gov (United States)

Beiert, Thomas; Tiyerili, Vedat; Knappe, Vincent; Effelsberg, Verena; Linhart, Markus; Stöckigt, Florian; Klein, Sabine; Schierwagen, Robert; Trebicka, Jonel; Nickenig, Georg; Schrickel, Jan W; Andrié, René P

2017-08-26

Relaxin-2 (RLX) is a peptide hormone that exerts beneficial anti-fibrotic and anti-inflammatory effects in diverse models of cardiovascular disease. The goal of this study was to determine the effects of RLX treatment on the susceptibility to atrial fibrillation (AF) after myocardial infarction (MI). Mice with cryoinfarction of the left anterior ventricular wall were treated for two weeks with either RLX (75 μg/kg/d) or vehicle (sodium acetate) delivered via subcutaneously implanted osmotic minipumps. RLX treatment significantly attenuated the increase in AF-inducibility following cryoinfarction and reduced the mean duration of AF episodes. Furthermore, epicardial mapping of both atria revealed an increase in conduction velocity. In addition to an attenuation of atrial hypertrophy, chronic application of RLX reduced atrial fibrosis, which was linked to a significant reduction in atrial mRNA expression of connective tissue growth factor. Transcript levels of the pro-inflammatory cytokines interleukin-6 and interleukin-1β were reduced in RLX treated mice, but macrophage infiltration into atrial myocardium was similar in the vehicle and RLX treated groups. Treatment with RLX in mice after MI reduces susceptibility to AF due to anti-inflammatory and anti-fibrotic properties. Because to these favorable actions, RLX may become a new therapeutic option in the treatment of AF, even when complicating MI. Copyright © 2017 Elsevier Inc. All rights reserved.

201Th chloride scintiscanning in myocardial infarction - correlation with ECG findings - diagnostic potential

International Nuclear Information System (INIS)

Kostka, I.

1980-01-01

The author intended to find out in how far myocardial scintiscanning with 201 Th chloride is a necessary auxiliary investigation in diagnosing acute myocardial infarction and whether there are correlations between ECG, increase of enzyme levels, and pressure measured in the lesser circulatory system. The scintiscans were evaluated by a new method: Defect sizes were determined using a transparent template and recorded in angular degrees. Also the reduced activity was considered. Especially posterior myocardial infarctions can be localized more easily and clearly by means of myocardial scintiscanning at rest, and also infarction sizes can be judged more easily. For a diagnosis of small myocardial infarctions or in patients with a block in their ECG picture, scintiscanning is a necessary part of the diagnostic spectrum. The findings of myocardial scintiscanning correspond well with those of other methods. As for the pressure increase in the lesser circulatory system, it is well correlated with the defect size shown by the scintiscan. 201 Th scintiscanning offers a good diagnostic possibility in those myocardial infarctions where ECG findings are ambiguous. (orig./MG) [de

 Effect of Thrombolytic Therapy on the Incidence of Early Left Ventricular Infarct Expansion in Acute Anterior Myocardial Infarction

Directory of Open Access Journals (Sweden)

Namir Ghanim Al-Tawil

2011-11-01

Full Text Available  Objectives: To determine the incidence of early left ventricular infarct expansion within five days after first anterior ST-segment elevation myocardial infarction and the effect of early thrombolytic therapy on the incidence of early infarct expansion compared with late thrombolytic therapy.Methods: In a prospective study of 101 patients (75males and 26 females, with the first attack of acute anterior myocardial infarction, their ages ranged from 40-80 years (mean age: 61.07±10.78 who had been admitted to the Coronary Care Unit of Hawler Teaching Hospital for the period from July 2007 through to September 2009. Those who received alteplase ≤3 hours of acute myocardial infarction were labelled as group-I (49 patients and those who received alteplase >3-12 hours were labelled as group-II (52 patients.Results: The incidence of early left ventricular infarct expansion was diagnosed by 2D-echocardiography and was found to be 17.8�20Group I patients had a lower incidence of early left ventricular infarct expansion (8.16�20compared with group-II (26.92�20 p=0.014. Patients with early left ventricular infarct expansion had a higher frequency rate of left ventricular systolic dysfunction (94.44�20compared to patients without early left ventricular infarct expansion (8.43�20p<0.001. There was a significant difference in the incidence of in-hospital mortality between the patients who developed early left ventricular infarct expansion (11.1�20compared with patients without early left ventricular infarct expansion (1.2�20p=0.025.Conclusion: Early reperfusion therapy in acute anterior myocardial infarction can decrease the incidence of early left ventricular infarct expansion, preserve left ventricular systolic function and decrease in-hospital mortality.

Gd-DTPA enhanced MRI of the brain infarction: correlation between onset of infarction and enhancing patterns

International Nuclear Information System (INIS)

Joo, An Young; Kim, Myung Soon; Lee, Sung Soo

1994-01-01

To evaluate the correlation between onset of brain infarction and Gd-DTPA enhancing patterns on MRI. We reviewed MRI of 58 lesions in 45 patients with clinically documented brain infarction retrospectively. Axial, coronal and sagittal T1WI (TR/TE 450-520/20), T2WI (TR/TE 2190/90) and Gd-DTPA enhanced T1WI were performed with a 0.5T superconductive MR system. We analyzed Gd-enhancing patterns that were divided into intravascular, meningeal, and parenchymal enhancement. Parenchymal pattern was subdivided into mottled, partial ring like and dense enhancement. Intravascular enhancement was seen at 1-10 days in 30(53%) of 58 infarctions. Meningeal enhancement (13%) was noted at 1-6 days. Parenchymal enhancement (50%) was seen at 2-28 days and subdividing patterns are as follows: The mottled enhancement pattern was seen earlier at 2-8 days and partial ring like or dense enhancement patterns at 5-28 days. After reviewing Gd-enhanced MRI of infarction, the intravascular and meningeal enhancement patterns were earlier than parenchymal enhancement. Among parenchymal patterns, the mottled pattern was seen earlier than partial ring like or dense patterns. In conclusion, Gd-enhancing patterns of brain infarction are useful in estimating the age of infarction including acute infarction

Occipital lobe infarctions are different

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Naess, Halvor; Waje-Andreassen, Ulrikke; Thomassen, Lars

2007-01-01

Halvor Naess, Ulrikke Waje-Andreassen, Lars ThomassenDepartment of Neurology, Haukeland University Hospital, University of Bergen, N-5021 Bergen, NorwayObjectives: We hypothesized that occipital lobe infarctions differ from infarctions in other locations as to etiology, risk factors and prognosis among young adults.Methods: Location, etiology, risk factors and long-term outcome were evaluated among all young adults 15–49 years suffering from cerebral infarction in Hordaland County, Norw...

Nepeta Dschuparensis Bornm Extract Moderates COX-2 and IL-1β Proteins in a Rat Model of Cerebral Ischemia

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Alireza Mousavi Nia

2017-03-01

Full Text Available Background: Nepeta dschuparensis Bornm (NP is used as a medicinal herb in Iran. In traditional medicine, this herb is extensively employed for curing ailments such as cardiovascular diseases. NP has antioxidant and anti-inflammatory properties. This project examined the effects of the NP extract on cyclooxygenase-2 (COX-2 and interleukin-1β (IL-1β protein levels and its efficacy in neuroprotection in a cerebral ischemia-reperfusion model. Methods: Twenty-six male rats were randomly divided into 3 groups: 1 sham (n=6: no middle cerebral artery occlusion (MCAO procedure, 2 control (n=10: MCAO procedure and treatment with normal saline, and 3 NP extract (n=10: MCAO procedure and treatment with the NP extract (20 mg/kg, i.p. at the beginning of reperfusion. To examine the injury caused by cerebral ischemia, we measured motor coordination and the infarct area using the rotarod test and triphenyl tetrazolium chloride staining, respectively. IL-1β and COX-2 protein levels, as inflammatory markers, were measured by immunoblotting assay. The statistical analyses were performed using SPSS, version 16, and the data are expressed as means±SEMs. Statistical difference was evaluated using the one-way ANOVA, followed by the post hoc LSD test (P<0.01. Results: Treatment with the NP extract significantly diminished the infarct volume and alleviated the motor coordination disorder induced by cerebral ischemia. The NP extract administration significantly attenuated the increase in IL-1β and COX-2 protein levels too (P<0.01. Conclusion: The beneficial effects of the NP extract are related to its ability to decrease the levels of IL-1β and COX-2.

Prognostic Value of the Thrombolysis in Myocardial Infarction Risk Score in ST-Elevation Myocardial Infarction Patients With Left Ventricular Dysfunction (from the EPHESUS Trial).

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Popovic, Batric; Girerd, Nicolas; Rossignol, Patrick; Agrinier, Nelly; Camenzind, Edoardo; Fay, Renaud; Pitt, Bertram; Zannad, Faiez

2016-11-15

The Thrombolysis in Myocardial Infarction (TIMI) risk score remains a robust prediction tool for short-term and midterm outcome in the patients with ST-elevation myocardial infarction (STEMI). However, the validity of this risk score in patients with STEMI with reduced left ventricular ejection fraction (LVEF) remains unclear. A total of 2,854 patients with STEMI with early coronary revascularization participating in the randomized EPHESUS (Epleronone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study) trial were analyzed. TIMI risk score was calculated at baseline, and its predictive value was evaluated using C-indexes from Cox models. The increase in reclassification of other variables in addition to TIMI score was assessed using the net reclassification index. TIMI risk score had a poor predictive accuracy for all-cause mortality (C-index values at 30 days and 1 year ≤0.67) and recurrent myocardial infarction (MI; C-index values ≤0.60). Among TIMI score items, diabetes/hypertension/angina, heart rate >100 beats/min, and systolic blood pressure model, lower LVEF, lower estimated glomerular filtration rate (eGFR), and previous MI were significantly associated with all-cause mortality. The predictive accuracy of this model, which included LVEF and eGFR, was fair for both 30-day and 1-year all-cause mortality (C-index values ranging from 0.71 to 0.75). In conclusion, TIMI risk score demonstrates poor discrimination in predicting mortality or recurrent MI in patients with STEMI with reduced LVEF. LVEF and eGFR are major factors that should not be ignored by predictive risk scores in this population. Copyright © 2016 Elsevier Inc. All rights reserved.

Using a Cloud Computing System to Reduce Door-to-Balloon Time in Acute ST-Elevation Myocardial Infarction Patients Transferred for Percutaneous Coronary Intervention.

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Ho, Chi-Kung; Chen, Fu-Cheng; Chen, Yung-Lung; Wang, Hui-Ting; Lee, Chien-Ho; Chung, Wen-Jung; Lin, Cheng-Jui; Hsueh, Shu-Kai; Hung, Shin-Chiang; Wu, Kuan-Han; Liu, Chu-Feng; Kung, Chia-Te; Cheng, Cheng-I

2017-01-01

This study evaluated the impact on clinical outcomes using a cloud computing system to reduce percutaneous coronary intervention hospital door-to-balloon (DTB) time for ST segment elevation myocardial infarction (STEMI). A total of 369 patients before and after implementation of the transfer protocol were enrolled. Of these patients, 262 were transferred through protocol while the other 107 patients were transferred through the traditional referral process. There were no significant differences in DTB time, pain to door of STEMI receiving center arrival time, and pain to balloon time between the two groups. Pain to electrocardiography time in patients with Killip I/II and catheterization laboratory to balloon time in patients with Killip III/IV were significantly reduced in transferred through protocol group compared to in traditional referral process group (both p cloud computing system in our present protocol did not reduce DTB time.

Striatocapsular infarction: MRI and MR angiography

Energy Technology Data Exchange (ETDEWEB)

Croisille, P. (Dept. of Neuroradiology, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon (France)); Turjman, F. (Dept. of Neuroradiology, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon (France)); Croisile, B. (Dept. of Neurology, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon (France)); Tournut, P. (Dept. of Neuroradiology, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon (France)); Laharotte, J.C. (Dept. of Neuroradiology, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon (France)); Aimard, G. (Dept. of Neurology, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon (France)); Trillet, M. (Dept. of Neurology, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon (France)); Duquesnel, J. (Dept. of Neuroradiology, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon (France)); Froment, J.C. (Dept. of Neuroradiology, Hopital Neurologique et Neurochirurgical Pierre

1994-08-01

We present a case of left striatocapsular infarction manifest clinically as a transient right hemiparesis. MRI showed a left striatocapsular infarct. Striatocapsular infarction, unlike lacunar infarction, is often associated with occlusive disease of the carotid artery. In order to screen the carotid vessels, cervical MR angiography (MRA) was performed during the same examination, demonstrating a left internal carotid artery occlusion, confirmed by contrast arteriography. MRA, a noninvasive modality, can be a useful adjunct to MRI, when diagnostic information concerning the cervical carotid artery is needed. (orig.)

Effect of thrombolytic therapy on exercise response during early recovery from acute myocardial infarction: a placebo controlled study

DEFF Research Database (Denmark)

Svendsen, Jesper Hastrup; Madsen, J K; Saunamäki, K I

1992-01-01

Several studies have shown that infarct size is reduced following thrombolytic treatment in patients with acute myocardial infarction. Exercise test variables, such as an impaired heart rate response during exercise, are known to be related to left ventricular function and patient prognosis follo...

Intravenous grafts of amniotic fluid-derived stem cells induce endogenous cell proliferation and attenuate behavioral deficits in ischemic stroke rats.

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Naoki Tajiri

Full Text Available We recently reported isolation of viable rat amniotic fluid-derived stem (AFS cells [1]. Here, we tested the therapeutic benefits of AFS cells in a rodent model of ischemic stroke. Adult male Sprague-Dawley rats received a 60-minute middle cerebral artery occlusion (MCAo. Thirty-five days later, animals exhibiting significant motor deficits received intravenous transplants of rat AFS cells or vehicle. At days 60-63 post-MCAo, significant recovery of motor and cognitive function was seen in stroke animals transplanted with AFS cells compared to vehicle-infused stroke animals. Infarct volume, as revealed by hematoxylin and eosin (H&E staining, was significantly reduced, coupled with significant increments in the cell proliferation marker, Ki67, and the neuronal marker, MAP2, in the dentate gyrus (DG [2] and the subventricular zone (SVZ of AFS cell-transplanted stroke animals compared to vehicle-infused stroke animals. A significantly higher number of double-labeled Ki67/MAP2-positive cells and a similar trend towards increased Ki67/MAP2 double-labeling were observed in the DG and SVZ of AFS cell-transplanted stroke animals, respectively, compared to vehicle-infused stroke animals. This study reports the therapeutic potential of AFS cell transplantation in stroke animals, possibly via enhancement of endogenous repair mechanisms.

Impact of Cardiovascular Events on Change in Quality of Life and Utilities in Patients After Myocardial Infarction

DEFF Research Database (Denmark)

Lewis, Eldrin F; Li, Yanhong; Pfeffer, Marc A

2014-01-01

infarction (MI). METHODS: The VALIANT (Valsartan In Acute Myocardial Infarction) trial enrolled 14,703 patients post-MI complicated by Killip class II or higher (scale measuring heart failure severity post-MI ranging from class I to IV) and/or reduced ejection fraction. The HRQL substudy included 2,556 (17...

Scintigraphic evaluation of suspected acute myocardial infarction

International Nuclear Information System (INIS)

Kan, M.K.; Hopkins, G.B.; Carroll, C.F.X.

1977-01-01

Ninety-one patients with chest pain suggestive of acute myocardial infarction were studied by static technetium /sup 99m/Tc stannous pyrophosphate scintigraphy and dynamic sodium pertechnetate /sup 99m/Tc cardioangiography. Twenty-three of 26 patients (88%) with acute transmural infarcts and 12 of 17 patients (71%) with nontransmural infarcts had abnormal static studies. In 45 patients with negative scintigrams, ECG or serum enzyme changes consistent with acute infarction failed to develop. Three false-positive static studies (6%) were recorded. Twenty of 43 (47%) patients with acute infarction had hemodynamic or structural abnormalities identified by cardioangiography. The dynamic study also proved helpful in localizing the site of infarction and in ruling out certain causes of false-positive static scintigrams

Diabetic muscle infarction: atypical MR appearance

International Nuclear Information System (INIS)

Sharma, P.; Mangwana, S.; Kapoor, R.K.

2000-01-01

We describe a case of diabetic muscle infarction which had atypical features of hyperintensity of the affected muscle on T1-weighted images. Biopsy was performed which revealed diffuse extensive hemorrhage within the infarcted muscle. We believe increased signal intensity on T1-weighted images should suggest hemorrhage within the infarcted muscle. (orig.)

Remote ischemic preconditioning fails to reduce infarct size in the Zucker fatty rat model of type-2 diabetes: role of defective humoral communication.

Science.gov (United States)

Wider, Joseph; Undyala, Vishnu V R; Whittaker, Peter; Woods, James; Chen, Xuequn; Przyklenk, Karin

2018-03-09

Remote ischemic preconditioning (RIPC), the phenomenon whereby brief ischemic episodes in distant tissues or organs render the heart resistant to infarction, has been exhaustively demonstrated in preclinical models. Moreover, emerging evidence suggests that exosomes play a requisite role in conveying the cardioprotective signal from remote tissue to the myocardium. However, in cohorts displaying clinically common comorbidities-in particular, type-2 diabetes-the infarct-sparing effect of RIPC may be confounded for as-yet unknown reasons. To investigate this issue, we used an integrated in vivo and in vitro approach to establish whether: (1) the efficacy of RIPC is maintained in the Zucker fatty rat model of type-2 diabetes, (2) the humoral transfer of cardioprotective triggers initiated by RIPC are transported via exosomes, and (3) diabetes is associated with alterations in exosome-mediated communication. We report that a standard RIPC stimulus (four 5-min episodes of hindlimb ischemia) reduced infarct size in normoglycemic Zucker lean rats, but failed to confer protection in diabetic Zucker fatty animals. Moreover, we provide novel evidence, via transfer of serum and serum fractions obtained following RIPC and applied to HL-1 cardiomyocytes subjected to hypoxia-reoxygenation, that diabetes was accompanied by impaired humoral communication of cardioprotective signals. Specifically, our data revealed that serum and exosome-rich serum fractions collected from normoglycemic rats attenuated hypoxia-reoxygenation-induced HL-1 cell death, while, in contrast, exosome-rich samples from Zucker fatty rats did not evoke protection in the HL-1 cell model. Finally, and unexpectedly, we found that exosome-depleted serum from Zucker fatty rats was cytotoxic and exacerbated hypoxia-reoxygenation-induced cardiomyocyte death.

Neuroprotective effect of agmatine in rats with transient cerebral ischemia using MR imaging and histopathologic evaluation.

Science.gov (United States)

Huang, Y C; Tzeng, W S; Wang, C C; Cheng, B C; Chang, Y K; Chen, H H; Lin, P C; Huang, T Y; Chuang, T J; Lin, J W; Chang, C P

2013-09-01

This study aimed to further investigate the effects of agmatine on brain edema in the rats with middle cerebral artery occlusion (MCAO) injury using magnetic resonance imaging (MRI) monitoring and biochemical and histopathologic evaluation. Following surgical induction of MCAO for 90min, agmatine was injected 5min after beginning of reperfusion and again once daily for the next 3 post-operative days. The events during ischemia and reperfusion were investigated by T2-weighted images (T2WI), serial diffusion-weighted images (DWI), calculated apparent diffusion coefficient (ADC) maps and contrast-enhanced T1-weighted images (CE-T1WI) during 3h-72h in a 1.5T Siemens MAGNETON Avanto Scanner. Lesion volumes were analyzed in a blinded and randomized manner. Triphenyltetrazolium chloride (TTC), Nissl, and Evans Blue stainings were performed at the corresponding sections. Increased lesion volumes derived from T2WI, DWI, ADC, CE-T1WI, and TTC all were noted at 3h and peaked at 24h-48h after MCAO injury. TTC-derived infarct volumes were not significantly different from the T2WI, DWI-, and CE-T1WI-derived lesion volumes at the last imaging time (72h) point except for significantly smaller ADC lesions in the MCAO model (Pagmatine-treated rats compared with the control ischemia rats (Pagmatine has neuroprotective effects against brain edema on a reperfusion model after transient cerebral ischemia. Copyright © 2013 Elsevier Inc. All rights reserved.

Minimizing infarct size. Annual scientific report, 1 Jul 1975--15 Apr 1976

International Nuclear Information System (INIS)

Braunwald, E.

1976-01-01

Several goals were achieved during this period of 9 months, both in the experimental laboratory and in patients with acute myocardial infarction. (1) A study of the effects of aprotinin administration on myocardial ischemic injury, subsequent necrosis and collateral blood flow following acute coronary artery occlusion was carried out to completion. (2) A study of the effect of cobra venom factor on myocardial necrosis was completed and the factors responsible for its action were examined. (3) A comparison was made of the effects of nitroglycerin and nitroprusside on ischemic injury and regional myocardial blood flow in patients with acute myocardial infarction and in dogs with coronary occlusions. (4) A method of direct measurement of infarct size in the rat was developed. It consists of occlusion of the main left coronary artery and the histologic quantification of the infarct at 48 hours and 3 weeks later by serial histologic sections or alternatively by measuring total left ventricular myocardial creative phosphokinase activity. (5) New electrocardiographic methods have been developed in order to evaluate atraumatically the extent of myocardial infarction in patients. (6) Intravenous injection of (113)mIn-ENTMP and (99m)TcENTMP in dogs following coronary artery occlusion permitted a sequential double labeling of the damaged myocardium. (7) Since hyaluronidase is a very effective drug in reducing myocardial damage both in the experimental animal and in patients with acute myocardial infarction, a study was carried out to ascertain its effects on collateral flow

Electroacupuncture-Induced Neuroprotection against Cerebral Ischemia in Rats: Role of the Dopamine D2 Receptor

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Ming-Shu Xu

2013-01-01

Full Text Available Background. Cerebral ischemia is known to produce brain damage and related behavioural deficits, including memory deficits and motor disorders. Evidence shows that EA significantly promotes recovery of neurological function and thus improves quality of life. Objective. Evidence exists for the involvement of catecholamines in human neuroplasticity. A better understanding of dopaminergic (DAergic modulation in this process will be important. Methods. A total of 72 adult male Sprague-Dawley (SD rats were divided into 6 groups: normal, model, EA, spiperone group, EA + spiperone group, and pergolide. The middle cerebral artery occlusion (MCAO model was used in all 6 groups except the normal group. A behavioural assessment was conducted at 1, 3, 5, and 7 days after MCAO. The percent of brain infarct area was also determined 7 days after MCAO. Tyrosine hydroxylase (TH and growth-associated protein 43 (GAP-43 fluorescence double labeling was performed in the striatum. Results. In this study, we found that EA at Fengchi (GB20 acupoints resulted in marked improvements based on a behavioural assessment. Both TTC staining and GAP-43 immunofluorescence labeling results showed that EA treatment reduced ischemia injury and promoted neuroplasticity compared with the model group. The D2R-selective agonist, pergolide, showed similar results, but these results were reversed by the D2R-selective antagonist, spiperone. We also found that there were more colocalization and expression of GAP-43 and TH in the EA and pergolide groups than those in the other groups. Conclusion. These results suggest that the neuroplasticity induced by EA was mediated by D2 autoreceptors in DAergic neurons.

Sacubitril and valsartan fixed combination to reduce heart failure events in post-acute myocardial infarction patients.

Science.gov (United States)

Zaid Iskandar, M; Lang, C C

2017-10-01

Heart failure is a term used to define a constellation of symptoms and signs that are commonly attributed to the inability of the heart to produce a cardiac output that meets the demands of the body. It remains a deadly disease, affecting between 1-2% of the population, and is more common in the elderly, with around 6-10% of patients over 65 suffering from the condition. Sacubitril/valsartan (LCZ-696) is a combined neprilysin inhibitor and angiotensin AT1 receptor blocker approved in recent years for the treatment of chronic heart failure with reduced ejection fraction. In an area where there have been limited pharmacological advances in the last 10 years, this drug was a game changer and a much welcomed addition to contemporary heart failure therapy. It is currently being studied in patients with heart failure with preserved ejection fraction and for the reduction of heart failure events post-acute myocardial infarction. Results from the ongoing PARADISE-MI study are awaited by the global cardiology community with great interest. Copyright 2017 Clarivate Analytics.

Mutual information and phase dependencies: measures of reduced nonlinear cardiorespiratory interactions after myocardial infarction.

Science.gov (United States)

Hoyer, Dirk; Leder, Uwe; Hoyer, Heike; Pompe, Bernd; Sommer, Michael; Zwiener, Ulrich

2002-01-01

The heart rate variability (HRV) is related to several mechanisms of the complex autonomic functioning such as respiratory heart rate modulation and phase dependencies between heart beat cycles and breathing cycles. The underlying processes are basically nonlinear. In order to understand and quantitatively assess those physiological interactions an adequate coupling analysis is necessary. We hypothesized that nonlinear measures of HRV and cardiorespiratory interdependencies are superior to the standard HRV measures in classifying patients after acute myocardial infarction. We introduced mutual information measures which provide access to nonlinear interdependencies as counterpart to the classically linear correlation analysis. The nonlinear statistical autodependencies of HRV were quantified by auto mutual information, the respiratory heart rate modulation by cardiorespiratory cross mutual information, respectively. The phase interdependencies between heart beat cycles and breathing cycles were assessed basing on the histograms of the frequency ratios of the instantaneous heart beat and respiratory cycles. Furthermore, the relative duration of phase synchronized intervals was acquired. We investigated 39 patients after acute myocardial infarction versus 24 controls. The discrimination of these groups was improved by cardiorespiratory cross mutual information measures and phase interdependencies measures in comparison to the linear standard HRV measures. This result was statistically confirmed by means of logistic regression models of particular variable subsets and their receiver operating characteristics.

Thrombolysis significantly reduces transient myocardial ischaemia following first acute myocardial infarction

DEFF Research Database (Denmark)

Mickley, H; Pless, P; Nielsen, J R

1992-01-01

In order to investigate whether thrombolysis affects residual myocardial ischaemia, we prospectively performed a predischarge maximal exercise test and early out-of-hospital ambulatory ST segment monitoring in 123 consecutive men surviving a first acute myocardial infarction (AMI). Seventy......-four patients fulfilled our criteria for thrombolysis, but only the last 35 patients included received thrombolytic therapy. As thrombolysis was not available in our Department at the start of the study, the first 39 patients included were conservatively treated (controls). No significant differences...... in baseline clinical characteristics were found between the two groups. In-hospital atrial fibrillation and digoxin therapy was more prevalent in controls (P less than 0.05). During exercise, thrombolysed patients reached a higher maximal work capacity compared with controls: 160 +/- 41 vs 139 +/- 34 W (P...

Omental Infarction Mimicking Cholecystitis

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David Smolilo

2015-01-01

Full Text Available Omental infarction can be difficult to diagnose preoperatively as imaging may be inconclusive and patients often present in a way that suggests a more common surgical pathology such as appendicitis. Here, a 40-year-old Caucasian man presented to casualty with shortness of breath and progressive right upper abdominal pain, accompanied with right shoulder and neck pain. Exploratory laparoscopy was eventually utilised to diagnose an atypical form of omental infarction that mimics cholecystitis. The vascular supply along the long axis of the segment was occluded initiating necrosis. In this case, the necrotic segment was adherent with the abdominal wall, a pathology not commonly reported in cases of omental infarction.

Dipyridamole induced directory disfunction of infarcted vessel, and estimation of patients with acute myocardial infarction and successful PTCA

International Nuclear Information System (INIS)

Hashimoto, Yasunori; Yamabe, Hiroshi; Kim, Sushik; Yano, Takashi; Fujita, Hideki; Kakimoto, Tetsuya; Namura, Hiroyuki; Maeda, Kazumi; Yokoyama, Mitsuhiro

1993-01-01

The purpose of this study was to determine whether transient disturbance of vascular dilation in the peripheral coronary vessels in patients with myocardial infarction in whom coronary recanalization was successfully attained in the acute stage. The subjects were 6 patients with acute myocardial infarction in whom recanalization was successfully attained without a significant coronary stenosis by emergency percutaneous transluminal coronary angioplasty (PTCA). Dipyridamole-loaded thallium-201 myocardial scintigraphy was undertaken during the acute stage (an average of 5 days after PTCA) and during convalescent stage (an average 24 days after PTCA). Defect was seen in the infarcted areas on early images during the acute stage in all 6 patients, and Tl uptake in the infarcted areas was improved during the convalescent stage in 2 of the 6 patients. In these two patients, fill-in phenomenon was seen in the infarcted area during acute stage when images were acquired after re-injection of Tl-201. These findings suggested that transient disturbance of vascular dilation may occur in the peripheral coronary artery vessels in the infarcted area where recanalization was successfully attained in patients with acute myocardial infarction. (N.K.)

Protein Synthesis Inhibition in the Peri-Infarct Cortex Slows Motor Recovery in Rats.

Science.gov (United States)

Schubring-Giese, Maximilian; Leemburg, Susan; Luft, Andreas Rüdiger; Hosp, Jonas Aurel

2016-01-01

Neuroplasticity and reorganization of brain motor networks are thought to enable recovery of motor function after ischemic stroke. Especially in the cortex surrounding the ischemic scar (i.e., peri-infarct cortex), evidence for lasting reorganization has been found at the level of neurons and networks. This reorganization depends on expression of specific genes and subsequent protein synthesis. To test the functional relevance of the peri-infarct cortex for recovery we assessed the effect of protein synthesis inhibition within this region after experimental stroke. Long-Evans rats were trained to perform a skilled-reaching task (SRT) until they reached plateau performance. A photothrombotic stroke was induced in the forelimb representation of the primary motor cortex (M1) contralateral to the trained paw. The SRT was re-trained after stroke while the protein synthesis inhibitor anisomycin (ANI) or saline were injected into the peri-infarct cortex through implanted cannulas. ANI injections reduced protein synthesis within the peri-infarct cortex by 69% and significantly impaired recovery of reaching performance through re-training. Improvement of motor performance within a single training session remained intact, while improvement between training sessions was impaired. ANI injections did not affect infarct size. Thus, protein synthesis inhibition within the peri-infarct cortex impairs recovery of motor deficits after ischemic stroke by interfering with consolidation of motor memory between training sessions but not short-term improvements within one session.

Cerebellar infarct patterns: The SMART-Medea study

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Laurens J.L. De Cocker, MD

2015-01-01

Conclusions: Small cerebellar infarcts proved to be much more common than larger infarcts, and preferentially involved the cortex. Small cortical infarcts predominantly involved the posterior lobes, showed sparing of subcortical white matter and occurred in characteristic topographic patterns.

The infarction patterns and the compensatory effect of collateral circulation in patients with internal carotid artery occlusion: a correlative study

International Nuclear Information System (INIS)

Gao Honghua; Wen Jiamei; Gao Lianbo

2012-01-01

Objective: To investigate the infarction patterns and the collateral circulation in patients with internal carotid artery occlusion with diffusion-weighted imaging and DSA, to analyze the mechanism of stroke caused by internal carotid artery occlusion and to discuss the correlation between the infarction patterns and the compensatory effect of collateral circulation. Methods: A total of 45 patients with acute cerebral infarction due to DSA-confirmed unilateral internal carotid artery occlusion, who were admitted to the hospital during the period from Jan. 2009 to Sep. 2010, were enrolled in this study. Diffusion-weighted imaging and DSA were performed in all patients. The infarction regions and the findings of PCoA/ACoA were recorded, and the ipsilateral infarction patterns were evaluated. The relationship between the infarction patterns and the compensatory effect of collateral circulation was statistically analyzed. Results: The ipsilateral infarction patterns caused by internal carotid artery occlusion were classified as small cortical infarcts (84.4%), internal watershed infarcts (48.9%), territory infarcts (46.7%), posterior watershed infarcts (22.2%), anterior watershed infarcts (13.3%), perforating artery infarcts (22.2%). Among them, 23 patients had small cortical infarcts together with cerebral watershed infarcts (60.5%). No territory infarcts were found in the patients with patent ACoA (0%, P=0.013), while 91.7% of the patients showing no patent PCoA and/or ACoA had territory infarcts (11/12, p=0.003). Conclusion: Both artery-to-artery embolism and hypoperfusion with impaired emboli clearance are involved in the mechanism of ipsilateral infarctions caused by internal carotid artery occlusion. Patent ACoA can reduce the incidence of territory infarcts, and it maybe protect patients from territory infarcts. (authors)

Patent foramen ovale closure with GORE HELEX or CARDIOFORM Septal Occluder vs. antiplatelet therapy for reduction of recurrent stroke or new brain infarct in patients with prior cryptogenic stroke: Design of the randomized Gore REDUCE Clinical Study.

Science.gov (United States)

Kasner, Scott E; Thomassen, Lars; Søndergaard, Lars; Rhodes, John F; Larsen, Coby C; Jacobson, Joth

2017-12-01

Rationale The utility of patent foramen ovale (PFO) closure for secondary prevention in patients with prior cryptogenic stroke is uncertain despite multiple randomized trials completed to date. Aims The Gore REDUCE Clinical Study (REDUCE) aims to establish superiority of patent foramen ovale closure in conjunction with antiplatelet therapy over antiplatelet therapy alone in reducing the risk of recurrent clinical ischemic stroke or new silent brain infarct in patients who have had a cryptogenic stroke. Methods and design This controlled, open-label trial randomized 664 subjects with cryptogenic stroke at 63 multinational sites in a 2:1 ratio to either antiplatelet therapy plus patent foramen ovale closure (with GORE® HELEX® Septal Occluder or GORE® CARDIOFORM Septal Occluder) or antiplatelet therapy alone. Subjects will be prospectively followed for up to five years. Neuroimaging is required for all subjects at baseline and at two years or study exit. Study outcomes The two co-primary endpoints for the study are freedom from recurrent clinical ischemic stroke through at least 24 months post-randomization and incidence of new brain infarct (defined as clinical ischemic stroke or silent brain infarct) through 24 months. The primary analyses are an unadjusted log-rank test and a binomial test of subject-based proportions, respectively, both on the intent-to-treat population, with adjustment for testing multiplicity. Discussion The REDUCE trial aims to target a patient population with truly cryptogenic strokes. Medical therapy is limited to antiplatelet agents in both arms thereby reducing confounding. The trial should determine whether patent foramen ovale closure with the Gore septal occluders is safe and more effective than medical therapy alone for the prevention of recurrent clinical ischemic stroke or new silent brain infarct; the neuroimaging data will provide an opportunity to further support the proof of concept. The main results are anticipated in 2017

Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial

NARCIS (Netherlands)

Hofmeijer, Jeannette; Kappelle, L. Jaap; Algra, Ale; Amelink, G. Johan; van Gijn, Jan; van der Worp, H. Bart; Algra, A.; Amelink, G. J.; van Gijn, J.; Hofmeijer, J.; Kappelle, L. J.; Macleod, M. R.; van der Worp, H. B.; de Bruijn, S. F. T. M.; Luijckx, G. J.; van Oostenbrugge, R.; Stam, J.; Boiten, J.; van der Graaf, Y.; Koudstaal, P. J.; Maas, A. I. R.; van Dijk, G. W.; Hacke, W.; Kalkman, C. J.; Tulleken, C. A. F.; Wijman, C. A. C.; van Buuren, M.

2009-01-01

BACKGROUND: Patients with space-occupying hemispheric infarctions have a poor prognosis, with case fatality rates of up to 80%. In a pooled analysis of randomised trials, surgical decompression within 48 h of stroke onset reduced case fatality and improved functional outcome; however, the effect of

Effect of 3-aminobenzamide, PARP inhibitor, on matrix metalloproteinase-9 level in plasma and brain of ischemic stroke model

International Nuclear Information System (INIS)

Koh, Seong-Ho; Chang, Dae-Il; Kim, Hee-Tae; Kim, Juhan; Kim, Myung-Ho; Kim, Kyung Suk; Bae, Inhee; Kim, Haekwon; Kim, Dong Won; Kim, Seung Hyun

2005-01-01

We investigated the effect of poly(ADP-ribose) polymerase (PARP) inhibitor on the levels of plasma and brain matrix metalloproteinase-9 (MMP-9) and the expression of nuclear factor kappa B (NF-κB) during experimental focal cerebral ischemia. The 3-aminobenzamide (3-AB), a PARP inhibitor, and saline were administered to 80 Sprague-Dawley rats [3-AB group; 5 rats for plasma sampling, 35 for brain sampling, and 40 for TTC staining] and to 85 rats (10, 35, and 40, respectively), respectively, 10 min before the occlusion of the left middle cerebral artery (MCAo) for 2 h. Infarct volume was measured by TTC staining, the serial levels of plasma and brain MMP-9 were measured by zymography just before and 2, 4, 8, 24, 48, and 72 h after MCAo, brain NF-κB activity was determined by Western blotting, and neutrophil infiltration was evaluated by assessing myeloperoxidase activity. Compared with control group, the levels of plasma and brain MMP-9, brain NF-κB, and MPO activities were significantly reduced in 3-AB group at each time point (p < 0.05). Plasma MMP-9 increased maximally at 4 h and then decreased rapidly, brain MMP-9 increased maximally at 24 h and persisted until 72 h, and NF-κB increased maximally at 24 h and then decreased slowly in both groups. Therefore, the PARP inhibitor reduces the expression of MMP-9 and NF-κB and the infiltration of neutrophils in ischemic stroke

Long-term post-stroke changes include myelin loss, specific deficits in sensory and motor behaviors and complex cognitive impairment detected using active place avoidance.

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Jin Zhou

Full Text Available Persistent neurobehavioral deficits and brain changes need validation for brain restoration. Two hours middle cerebral artery occlusion (tMCAO or sham surgery was performed in male Sprague-Dawley rats. Neurobehavioral and cognitive deficits were measured over 10 weeks included: (1 sensory, motor, beam balance, reflex/abnormal responses, hindlimb placement, forepaw foot fault and cylinder placement tests, and (2 complex active place avoidance learning (APA and simple passive avoidance retention (PA. Electroretinogram (ERG, hemispheric loss (infarction, hippocampus CA1 neuronal loss and myelin (Luxol Fast Blue staining in several fiber tracts were also measured. In comparison to Sham surgery, tMCAO surgery produced significant deficits in all behavioral tests except reflex/abnormal responses. Acute, short lived deficits following tMCAO were observed for forelimb foot fault and forelimb cylinder placement. Persistent, sustained deficits for the whole 10 weeks were exhibited for motor (p<0.001, sensory (p<0.001, beam balance performance (p<0.01 and hindlimb placement behavior (p<0.01. tMCAO produced much greater and prolonged cognitive deficits in APA learning (maximum on last trial of 604±83% change, p<0.05 but only a small, comparative effect on PA retention. Hemispheric loss/atrophy was measured 10 weeks after tMCAO and cross-validated by two methods (e.g., almost identical % ischemic hemispheric loss of 33.4±3.5% for H&E and of 34.2±3.5% for TTC staining. No visual dysfunction by ERG and no hippocampus neuronal loss were detected after tMCAO. Fiber tract damage measured by Luxol Fast Blue myelin staining intensity was significant (p<0.01 in the external capsule and striatum but not in corpus callosum and anterior commissure. In summary, persistent neurobehavioral deficits were validated as important endpoints for stroke restorative research in the future. Fiber myelin loss appears to contribute to these long term behavioral dysfunctions and

Electroacupunctre improves motor impairment via inhibition of microglia-mediated neuroinflammation in the sensorimotor cortex after ischemic stroke.

Science.gov (United States)

Liu, Weilin; Wang, Xian; Yang, Shanli; Huang, Jia; Xue, Xiehua; Zheng, Yi; Shang, Guanhao; Tao, Jing; Chen, Lidian

2016-04-15

Electroacupuncture (EA) is one of the safety and effective therapies for improving neurological and sensorimotor impairment via blockade of inappropriate inflammatory responses. However, the mechanisms of anti-inflammation involved is far from been fully elucidated. Focal cerebral ischemic stroke was administered by the middle cerebral artery occlusion and reperfusion (MCAO/R) surgery. The MCAO/R rats were accepted EA treatment at the LI 11 and ST 36 acupoints for consecutive 3days. The neurological outcome, animal behaviors test and molecular biology assays were used to evaluate the MCAO/R model and therapeutic effect of EA. EA treatment for MCAO rats showed a significant reduction in the infarct volumes accompanied by functional recovery in mNSS outcomes, motor function performances. The possible mechanisms that EA treatment attenuated the over-activation of Iba-1 and ED1 positive microglia in the peri-infract sensorimotor cortex. Simultaneously, both tissue and serum protein levels of the tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) were decreased by EA treatment in MCAO/R injured rats. The levels of inflammatory cytokine tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) were decreased in the peri-infract sensorimotor cortex and blood serum of MCAO/R injured rats after EA treatment. Furthermore, we found that EA treatment prevented from the nucleus translocation of NF-κB p65 and suppressed the expression of p38 mitogen-activated protein kinase (p38 MAPK) and myeloid differentiation factor 88 (MyD88) in the peri-infract sensorimotor cortex. The findings from this study indicated that EA improved the motor impairment via inhibition of microglia-mediated neuroinflammation that invoked NF-κB p65, p38 MAPK and MyD88 produced proinflammatory cytokine in the peri-infract sensorimotor cortex of rats following ischemic stroke. Copyright © 2016 Elsevier Inc. All rights reserved.

The Post-Myocardial Infarction Pacing Remodeling Prevention Therapy (PRomPT) Trial

DEFF Research Database (Denmark)

Chung, Eugene S; Fischer, Trent M; Kueffer, Fred

2015-01-01

BACKGROUND: Despite considerable improvements in the medical management of patients with myocardial infarction (MI), patients with large MI still have substantial risk of developing heart failure. In the early post-MI setting, implantable cardioverter defibrillators have reduced arrhythmic deaths...

Difference in MRI findings and risk factors between multiple infarction without dementia and multi-infarct dementia

International Nuclear Information System (INIS)

Yanagisawa, Masashi; Kaieda, Makoto; Nagatsumi, Atsushi; Terashi, Akiro

1995-01-01

MRI findings and risk factors for vascular dementia were evaluated with multi-variate analysis in 96 multi-infarct patients without dementia and 40 multi-infarct patients with dementia (MID). Only subjects with small infarcts in the territory of the perforator artery or deep white matter were studied. The diagnosis of MID was diagnosed according to DMS-III criteria and Hachinski's ischemia score. Location and area of patchy high-intensity areas including small infarcts, the degree of periventricular high intensity (PVH), and the degree of brain atrophy were examined with MR images. Independent variables were: history of hypertension, diabetes mellitus, other complications; systolic and diastolic blood pressure, atherosclerotic index, hematocrit, history of smoking, level of education, and activities of daily life (ADL). Hayashi's quantification method II was used to analyze the data. The most significant correlation was found between history of hypertension and dementia (partial correlation coefficient: 0.39). Significant correlations were also found between ADL and dementia (0.32), between thalamic infarction and dementia (0.31), and between PVH and dementia (0.27). Age, brain atrophy index, and history of diabetes mellitus contributed little to dementia. The contribution to dementia did not differ significantly between right and left patchy high-intensity areas on MR images. Location of infarcts, except for bilateral thalamic infarcts and large PVH, contributed little to dementia. Thus it would be difficult to base a prediction of the prevalence of vascular dementia on MRI findings. However, both hypertention and ADL contribute to vascular dementia and both are treatable, which may be significant for the prevention of dementia. (author)

[The radiological findings of caisson-induced bone infarcts. The relationship between acute arthralgia and bone infarcts (author's transl)].

Science.gov (United States)

Horváth, V F

1978-07-01

The radiological features, such as calcification in long bones due to infarcts, resulting from Caisson disease are described by the author on the basis of an extensive experience. The similar localisation of acute "arthralgia" and bone infarcts make it appear probable that the infarcts play a primary role in the production of "osteo-articular" pain. The author stresses the advisability of examining the adjacent portions of the tibia and femur at the initial pre-employment examination, since bone infarcts can be caused by a variety of conditions other than work in Caissons.

Therapeutic effect of a novel Wnt pathway inhibitor on cardiac regeneration after myocardial infarction.

Science.gov (United States)

Yang, Dezhong; Fu, Wenbin; Li, Liangpeng; Xia, Xuewei; Liao, Qiao; Yue, Rongchuan; Chen, Hongmei; Chen, Xiongwen; An, Songzhu; Zeng, Chunyu; Wang, Wei Eric

2017-12-15

After myocardial infarction (MI), the heart is difficult to repair because of great loss of cardiomyoctyes and lack of cardiac regeneration. Novel drug candidates that aim at reducing pathological remodeling and stimulating cardiac regeneration are highly desirable. In the present study, we identified if and how a novel porcupine inhibitor CGX1321 influenced MI and cardiac regeneration. Permanent ligation of left anterior descending (LAD) coronary artery was performed in mice to induce MI injury. Cardiac function was measured by echocardiography, infarct size was examined by TTC staining. Fibrosis was evaluated with Masson's trichrome staining and vimentin staining. As a result, CGX1321 administration blocked the secretion of Wnt proteins, and inhibited both canonical and non-canonical Wnt signaling pathways. CGX1321 improved cardiac function, reduced myocardial infarct size, and fibrosis of post-MI hearts. CGX1321 significantly increased newly formed cardiomyocytes in infarct border zone of post-MI hearts, evidenced by the increased EdU + cardiomyocytes. Meanwhile, CGX1321 increased Ki67 + and phosphohistone H3 (PH3 + ) cardiomyocytes in culture, indicating enhanced cardiomyocyte proliferation. The mRNA microarray showed that CGX1321 up-regulated cell cycle regulating genes such as Ccnb1 and Ccne1 CGX1321 did not alter YAP protein phosphorylation and nuclear translocation in cardiomyocytes. In conclusion, porcupine inhibitor CGX1321 reduces MI injury by limiting fibrosis and promoting regeneration. It promotes cardiomyocyte proliferation by stimulating cell cycle regulating genes with a Hippo/YAP-independent pathway. © 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

The Pathogenesis of Human Myocardial Infarction

Science.gov (United States)

Rona, George

1966-01-01

Coronary arteriography, dissection of the coronary arteries and histopathological examination of the heart were carried out in 150 autopsies to study the effect of coronary narrowing and occlusion, of the presence of collaterals, and of coronary artery predominance on the development of myocardial infarction. The thrombosis rate was related to the severity of coronary sclerosis. The development of collaterals was not enhanced by coronary sclerosis and occlusion, and collaterals did not protect the myocardium against reinfarction. Coronary occlusion was regularly demonstrable in recent myocardial infarct cases. The association of atrial and posterior ventricular infarcts was explained by occlusion of their common arterial branch. The interdependence between coronary sclerosis, thrombosis and myocardial infarction in human autopsy material emphasizes the importance of mural coronary artery disease in the genesis of coronary occlusion and myocardial infarction, and it is at variance with statistical data and experimental results. ImagesFig. 1Fig. 2Fig. 3Fig. 4Fig. 5Fig. 6 PMID:5924947

Increased matrix metalloproteinase-8 and -9 activity in patients with infarct rupture after myocardial infarction

NARCIS (Netherlands)

Borne, S.W.M. van den; Cleutjens, J.P.M.; Hanemaaijer, R.; Creemers, E.E.; Smits, J.F.M.; Daemen, M.J.A.P.; Blankesteijn, W.M.

2009-01-01

Background: Infarct rupture is a usually fatal complication of myocardial infarction (MI), for which no molecular mechanism has been described in humans. Experimental evidence in mouse models suggests that the degradation of the extracellular matrix by matrix metalloproteinases (MMPs) plays an

Orbital infarction in sickle cell disease

International Nuclear Information System (INIS)

Wolff, M.H.; Sty, J.R.

1985-01-01

Bone infarction is common in sickle cell disease; however, involvement of the orbit is not. Only four cases have been reported in the English literature. We describe a patient who presented with headache, proptosis and lid edema due to infarction of the sphenoid bone. The combination of radionuclide bone imaging and computed tomography (CT) of the orbit were useful in differentiating bone infarction from other etiologies of proptosis. (orig.)

The Systematic Evaluation of Identifying the Infarct Related Artery Utilizing Cardiac Magnetic Resonance in Patients Presenting with ST-Elevation Myocardial Infarction.

Directory of Open Access Journals (Sweden)

Carine E Hamo

Full Text Available Identification of the infarct-related artery (IRA in patients with STEMI using coronary angiography (CA is often based on the ECG and can be challenging in patients with severe multi-vessel disease. The current study aimed to determine how often percutaneous intervention (PCI is performed in a coronary artery different from the artery supplying the territory of acute infarction on cardiac magnetic resonance imaging (CMR.We evaluated 113 patients from the Reduction of infarct Expansion and Ventricular remodeling with Erythropoetin After Large myocardial infarction (REVEAL trial, who underwent CMR within 4±2 days of revascularization. Blinded reviewers interpreted CA to determine the IRA and CMR to determine the location of infarction on a 17-segment model. In patients with multiple infarcts on CMR, acuity was determined with T2-weighted imaging and/or evidence of microvascular obstruction.A total of 5 (4% patients were found to have a mismatch between the IRA identified on CMR and CA. In 4/5 cases, there were multiple infarcts noted on CMR. Thirteen patients (11.5% had multiple infarcts in separate territories on CMR with 4 patients (3.5% having multiple acute infarcts and 9 patients (8% having both acute and chronic infarcts.In this select population of patients, the identification of the IRA by CA was incorrect in 4% of patients presenting with STEMI. Four patients with a mismatch had an acute infarction in more than one coronary artery territory on CMR. The role of CMR in patients presenting with STEMI with multi-vessel disease on CA deserves further investigation.

CT findings of early acute cerebral infarction

International Nuclear Information System (INIS)

Kim, Tae Hoon; Choi, Woo Suk; Ryu, Kyung Nam

1992-01-01

The CT findings of the acute cerebral infarction are well known. However the CT findings of early stroke within 24 hours of the onset have not been sufficiently reported. The purpose of this study is to evaluate early acute cerebral infarction on CT within 24 hours after ictus. The early and accurate CT diagnosis could lead to the appropriate therapy and improved outcome of the patients. Authors retrospectively analyzed 16 patients with early acute cerebral infarction. Acute cerebral infarction was confirmed by follow-up CT in 11 patients, SPECT in 4 patients, and MRI in 1 patient. The CT findings of early acute cerebral infarction include effacement of cortical sulci or cistern (n = 16, 100%), hyperattenuation of MCA (n = 3), obscuration of lentiform nucleus (n = 6), loss of insular ribbon (n = 6) and subtle low density in hemisphere (n = 5). The most frequent finding was effacement of cortical sulci in our study, and it was thought to be the most important sign of early acute cerebral infarction

CT findings of early acute cerebral infarction

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Kim, Tae Hoon; Choi, Woo Suk; Ryu, Kyung Nam [Kyung Hee University Hospital, Seoul (Korea, Republic of)

1992-11-15

The CT findings of the acute cerebral infarction are well known. However the CT findings of early stroke within 24 hours of the onset have not been sufficiently reported. The purpose of this study is to evaluate early acute cerebral infarction on CT within 24 hours after ictus. The early and accurate CT diagnosis could lead to the appropriate therapy and improved outcome of the patients. Authors retrospectively analyzed 16 patients with early acute cerebral infarction. Acute cerebral infarction was confirmed by follow-up CT in 11 patients, SPECT in 4 patients, and MRI in 1 patient. The CT findings of early acute cerebral infarction include effacement of cortical sulci or cistern (n = 16, 100%), hyperattenuation of MCA (n = 3), obscuration of lentiform nucleus (n = 6), loss of insular ribbon (n = 6) and subtle low density in hemisphere (n = 5). The most frequent finding was effacement of cortical sulci in our study, and it was thought to be the most important sign of early acute cerebral infarction.

Acute myocardial infarction: Can it be a complication of acute organophosphorus compound poisoning?

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P Joshi

2013-01-01

Full Text Available Organophosphorus compounds are used as pesticides and represent a common cause of poisoning in developing countries including India due to their widespread availability and use. Toxicity due to these agents can affect many organs including heart. Here, we report a case of acute organophosphorus poisoning (parathion, followed by acute myocardial infarction; documented by clinical features, electrocardiographic changes, and elevated cardiac enzymes. Myocardial infarction has been rarely reported with organophosphorus compounds exposure, thus awareness of this complication can reduce morbidity and mortality.

LXW7 ameliorates focal cerebral ischemia injury and attenuates inflammatory responses in activated microglia in rats

International Nuclear Information System (INIS)

Fang, T.; Zhou, D.; Lu, L.; Tong, X.; Wu, J.; Yi, L.

2016-01-01

Inflammation plays a pivotal role in ischemic stroke, when activated microglia release excessive pro-inflammatory mediators. The inhibition of integrin αvβ3 improves outcomes in rat focal cerebral ischemia models. However, the mechanisms by which microglia are neuroprotective remain unclear. This study evaluated whether post-ischemic treatment with another integrin αvβ3 inhibitor, the cyclic arginine-glycine-aspartic acid (RGD) peptide-cGRGDdvc (LXW7), alleviates cerebral ischemic injury. The anti-inflammatory effect of LXW7 in activated microglia within rat focal cerebral ischemia models was examined. A total of 108 Sprague-Dawley rats (250–280 g) were subjected to middle cerebral artery occlusion (MCAO). After 2 h, the rats were given an intravenous injection of LXW7 (100 μg/kg) or phosphate-buffered saline (PBS). Neurological scores, infarct volumes, brain water content (BWC) and histology alterations were determined. The expressions of pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β)], and Iba1-positive activated microglia, within peri-ischemic brain tissue, were assessed with ELISA, western blot and immunofluorescence staining. Infarct volumes and BWC were significantly lower in LXW7-treated rats compared to those in the MCAO + PBS (control) group. The LXW7 treatment lowered the expression of pro-inflammatory cytokines. There was a reduction of Iba1-positive activated microglia, and the TNF-α and IL-1β expressions were attenuated. However, there was no difference in the Zea Longa scores between the ischemia and LXW7 groups. The results suggest that LXW7 protected against focal cerebral ischemia and attenuated inflammation in activated microglia. LXW7 may be neuroprotective during acute MCAO-induced brain damage and microglia-related neurodegenerative diseases

Fatty acid methyl esters and Solutol HS 15 confer neuroprotection after focal and global cerebral ischemia.

Science.gov (United States)

Lin, Hung Wen; Saul, Isabel; Gresia, Victoria L; Neumann, Jake T; Dave, Kunjan R; Perez-Pinzon, Miguel A

2014-02-01

We previously showed that palmitic acid methyl ester (PAME) and stearic acid methyl ester (SAME) are simultaneously released from the sympathetic ganglion and PAME possesses potent vasodilatory properties which may be important in cerebral ischemia. Since PAME is a potent vasodilator simultaneously released with SAME, our hypothesis was that PAME/SAME confers neuroprotection in rat models of focal/global cerebral ischemia. We also examined the neuroprotective properties of Solutol HS15, a clinically approved excipient because it possesses similar fatty acid compositions as PAME/SAME. Asphyxial cardiac arrest (ACA, 6 min) was performed 30 min after PAME/SAME treatment (0.02 mg/kg, IV). Solutol HS15 (2 ml/kg, IP) was injected chronically for 14 days (once daily). Histopathology of hippocampal CA1 neurons was assessed 7 days after ACA. For focal ischemia experiments, PAME, SAME, or Solutol HS15 was administered following reperfusion after 2 h of middle cerebral artery occlusion (MCAO). 2,3,5-Triphenyltetrazolium staining of the brain was performed 24 h after MCAO and the infarct volume was quantified. Following ACA, the number of surviving hippocampal neurons was enhanced by PAME-treated (68%), SAME-treated (69%), and Solutol-treated HS15 (68%) rats as compared to ACA only-treated groups. Infarct volume was decreased by PAME (83%), SAME (68%), and Solutol HS15 (78%) as compared to saline (vehicle) in MCAO-treated animals. PAME, SAME, and Solutol HS15 provide robust neuroprotection in both paradigms of ischemia. This may prove therapeutically beneficial since Solutol HS15 is already administered as a solublizing agent to patients. With proper timing and dosage, administration of Solutol HS15 and PAME/SAME can be an effective therapy against cerebral ischemia.

LXW7 ameliorates focal cerebral ischemia injury and attenuates inflammatory responses in activated microglia in rats

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Fang, T.; Zhou, D.; Lu, L.; Tong, X.; Wu, J.; Yi, L. [Department of Neurology, Shenzhen Hospital, Peking University, Shenzhen (China)

2016-08-01

Inflammation plays a pivotal role in ischemic stroke, when activated microglia release excessive pro-inflammatory mediators. The inhibition of integrin αvβ3 improves outcomes in rat focal cerebral ischemia models. However, the mechanisms by which microglia are neuroprotective remain unclear. This study evaluated whether post-ischemic treatment with another integrin αvβ3 inhibitor, the cyclic arginine-glycine-aspartic acid (RGD) peptide-cGRGDdvc (LXW7), alleviates cerebral ischemic injury. The anti-inflammatory effect of LXW7 in activated microglia within rat focal cerebral ischemia models was examined. A total of 108 Sprague-Dawley rats (250–280 g) were subjected to middle cerebral artery occlusion (MCAO). After 2 h, the rats were given an intravenous injection of LXW7 (100 μg/kg) or phosphate-buffered saline (PBS). Neurological scores, infarct volumes, brain water content (BWC) and histology alterations were determined. The expressions of pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β)], and Iba1-positive activated microglia, within peri-ischemic brain tissue, were assessed with ELISA, western blot and immunofluorescence staining. Infarct volumes and BWC were significantly lower in LXW7-treated rats compared to those in the MCAO + PBS (control) group. The LXW7 treatment lowered the expression of pro-inflammatory cytokines. There was a reduction of Iba1-positive activated microglia, and the TNF-α and IL-1β expressions were attenuated. However, there was no difference in the Zea Longa scores between the ischemia and LXW7 groups. The results suggest that LXW7 protected against focal cerebral ischemia and attenuated inflammation in activated microglia. LXW7 may be neuroprotective during acute MCAO-induced brain damage and microglia-related neurodegenerative diseases.

Enhanced expressions of microvascular smooth muscle receptors after focal cerebral ischemia occur via the MAPK MEK/ERK pathway

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Edvinsson Lars

2008-09-01

Full Text Available Abstract Background MEK1/2 is a serine/threonine protein that phosphorylates extracellular signal-regulated kinase (ERK1/2. Cerebral ischemia results in enhanced expression of cerebrovascular contractile receptors in the middle cerebral artery (MCA leading to the ischemic region. Here we explored the role of the MEK/ERK pathway in receptor expression following ischemic brain injury using the specific MEK1 inhibitor U0126. Methods and result Rats were subjected to a 2-h middle cerebral artery occlusion (MCAO followed by reperfusion for 48-h and the ischemic area was calculated. The expression of phosphorylated ERK1/2 and Elk-1, and of endothelin ETA and ETB, angiotensin AT1, and 5-hydroxytryptamine 5-HT1B receptors were analyzed with immunohistochemistry using confocal microscopy in cerebral arteries, microvessels and in brain tissue. The expression of endothelin ETB receptor was analyzed by quantitative Western blot. We demonstrate that there is an increase in the number of contractile smooth muscle receptors in the MCA and in micro- vessels within the ischemic region. The enhanced expression occurs in the smooth muscle cells as verified by co-localization studies. This receptor upregulation is furthermore associated with enhanced expression of pERK1/2 and of transcription factor pElk-1 in the vascular smooth muscle cells. Blockade of transcription with the MEK1 inhibitor U0126, given at the onset of reperfusion or as late as 6 hours after the insult, reduced transcription (pERK1/2 and pElk-1, the enhanced vascular receptor expression, and attenuated the cerebral infarct and improved neurology score. Conclusion Our results show that MCAO results in upregulation of cerebrovascular ETB, AT1 and 5-HT1B receptors. Blockade of this event with a MEK1 inhibitor as late as 6 h after the insult reduced the enhanced vascular receptor expression and the associated cerebral infarction.

Hippo pathway deficiency reverses systolic heart failure after infarction.

Science.gov (United States)

Leach, John P; Heallen, Todd; Zhang, Min; Rahmani, Mahdis; Morikawa, Yuka; Hill, Matthew C; Segura, Ana; Willerson, James T; Martin, James F

2017-10-12

Mammalian organs vary widely in regenerative capacity. Poorly regenerative organs, such as the heart are particularly vulnerable to organ failure. Once established, heart failure commonly results in mortality. The Hippo pathway, a kinase cascade that prevents adult cardiomyocyte proliferation and regeneration, is upregulated in human heart failure. Here we show that deletion of the Hippo pathway component Salvador (Salv) in mouse hearts with established ischaemic heart failure after myocardial infarction induces a reparative genetic program with increased scar border vascularity, reduced fibrosis, and recovery of pumping function compared with controls. Using translating ribosomal affinity purification, we isolate cardiomyocyte-specific translating messenger RNA. Hippo-deficient cardiomyocytes have increased expression of proliferative genes and stress response genes, such as the mitochondrial quality control gene, Park2. Genetic studies indicate that Park2 is essential for heart repair, suggesting a requirement for mitochondrial quality control in regenerating myocardium. Gene therapy with a virus encoding Salv short hairpin RNA improves heart function when delivered at the time of infarct or after ischaemic heart failure following myocardial infarction was established. Our findings indicate that the failing heart has a previously unrecognized reparative capacity involving more than cardiomyocyte renewal.

Electroacupuncture acutely improves cerebral blood flow and attenuates moderate ischemic injury via an endothelial mechanism in mice.

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Ji Hyun Kim

Full Text Available Electroacupuncture (EA is a novel therapy based on traditional acupuncture combined with modern eletrotherapy that is currently being investigated as a treatment for acute ischemic stroke. Here, we studied whether acute EA stimulation improves tissue and functional outcome following experimentally induced cerebral ischemia in mice. We hypothesized that endothelial nitric oxide synthase (eNOS-mediated perfusion augmentation was related to the beneficial effects of EA by interventions in acute ischemic injury. EA stimulation at Baihui (GV20 and Dazhui (GV14 increased cerebral perfusion in the cerebral cortex, which was suppressed in eNOS KO, but there was no mean arterial blood pressure (MABP response. The increased perfusion elicited by EA were completely abolished by a muscarinic acetylcholine receptor (mAChR blocker (atropine, but not a β-adrenergic receptor blocker (propranolol, an α-adrenergic receptor blocker (phentolamine, or a nicotinic acetylcholine receptor (nAChR blocker (mecamylamine. In addition, EA increased acetylcholine (ACh release and mAChR M3 expression in the cerebral cortex. Acute EA stimulation after occlusion significantly reduced infarct volume by 34.5% when compared to a control group of mice at 24 h after 60 min-middle cerebral artery occlusion (MCAO (moderate ischemic injury, but not 90-min MCAO (severe ischemic injury. Furthermore, the impact of EA on moderate ischemic injury was totally abolished in eNOS KO. Consistent with a smaller infarct size, acute EA stimulation led to prominent improvement of neurological function and vestibule-motor function. Our results suggest that acute EA stimulation after moderate focal cerebral ischemia, but not severe ischemia improves tissue and functional recovery and ACh/eNOS-mediated perfusion augmentation might be related to these beneficial effects of EA by interventions in acute ischemic injury.

Molecular Mechanisms Responsible for Neuron-Derived Conditioned Medium (NCM-Mediated Protection of Ischemic Brain.

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Chi-Hsin Lin

Full Text Available The protective value of neuron-derived conditioned medium (NCM in cerebral ischemia and the underlying mechanism(s responsible for NCM-mediated brain protection against cerebral ischemia were investigated in the study. NCM was first collected from the neuronal culture growing under the in vitro ischemic condition (glucose-, oxygen- and serum-deprivation or GOSD for 2, 4 or 6 h. Through the focal cerebral ischemia (bilateral CCAO/unilateral MCAO animal model, we discovered that ischemia/reperfusion (I/R-induced brain infarction was significantly reduced by NCM, given directly into the cistern magna at the end of 90 min of CCAO/MCAO. Immunoblocking and chemical blocking strategies were applied in the in vitro ischemic studies to show that NCM supplement could protect microglia, astrocytes and neurons from GOSD-induced cell death, in a growth factor (TGFβ1, NT-3 and GDNF and p-ERK dependent manner. Brain injection with TGFβ1, NT3, GDNF and ERK agonist (DADS alone or in combination, therefore also significantly decreased the infarct volume of ischemic brain. Moreover, NCM could inhibit ROS but stimulate IL-1β release from GOSD-treated microglia and limit the infiltration of IL-β-positive microglia into the core area of ischemic brain, revealing the anti-oxidant and anti-inflammatory activities of NCM. In overall, NCM-mediated brain protection against cerebral ischemia has been demonstrated for the first time in S.D. rats, due to its anti-apoptotic, anti-oxidant and potentially anti-glutamate activities (NCM-induced IL-1β can inhibit the glutamate-mediated neurotoxicity and restriction upon the infiltration of inflammatory microglia into the core area of ischemic brain. The therapeutic potentials of NCM, TGFβ1, GDNF, NT-3 and DADS in the control of cerebral ischemia in human therefore have been suggested and require further investigation.

Rationale and design of a double-blind, multicenter, randomized, placebo-controlled clinical trial of early administration of intravenous beta-blockers in patients with ST-elevation myocardial infarction before primary percutaneous coronary intervention : EARLY beta-blocker Administration before primary PCI in patients with ST-elevation Myocardial Infarction trial

NARCIS (Netherlands)

Roolvink, Vincent; Rasoul, Saman; Ottervanger, Jan Paul; Dambrink, Jan-Henk E.; Lipsic, Erik; van der Horst, Iwan C. C.; de Smet, Bart; Kedhi, Elvin; Gosselink, A. T. Marcel; Piek, Jan J.; Sanchez-Brunete, Vicente; Ibanez, Borja; Fuster, Valentin; van't Hof, Arnoud W. J.

2014-01-01

Background beta-Blockers have a class 1a recommendation in the treatment of patients with ST-elevation myocardial infarctions (STEMIs), as they are associated with a reduced mortality, recurrent myocardial infarction, life-threatening arrhythmias, and with prevention of unfavorable left ventricular

Cerebellar cortical infarct cavities and vertebral artery disease

Energy Technology Data Exchange (ETDEWEB)

Cocker, Laurens J.L. de [University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands); Kliniek Sint-Jan Radiologie, Brussels (Belgium); Compter, A.; Kappelle, L.J.; Worp, H.B. van der [University Medical Center Utrecht, Department of Neurology and Neurosurgery, Brain Center Rudolf Magnus, Utrecht (Netherlands); Luijten, P.R.; Hendrikse, J. [University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands)

2016-09-15

Cerebellar cortical infarct cavities are a newly recognised entity associated with atherothromboembolic cerebrovascular disease and worse physical functioning. We aimed to investigate the relationship of cerebellar cortical infarct cavities with symptomatic vertebrobasilar ischaemia and with vascular risk factors. We evaluated the MR images of 46 patients with a recent vertebrobasilar TIA or stroke and a symptomatic vertebral artery stenosis ≥50 % from the Vertebral Artery Stenting Trial (VAST) for the presence of cerebellar cortical infarct cavities ≤1.5 cm. At inclusion in VAST, data were obtained on age, sex, history of vertebrobasilar TIA or stroke, and vascular risk factors. Adjusted risk ratios were calculated with Poisson regression analyses for the relation between cerebellar cortical infarct cavities and vascular risk factors. Sixteen out of 46 (35 %) patients showed cerebellar cortical infarct cavities on the initial MRI, and only one of these 16 patients was known with a previous vertebrobasilar TIA or stroke. In patients with symptomatic vertebrobasilar ischaemia, risk factor profiles of patients with cerebellar cortical infarct cavities were not different from patients without these cavities. Cerebellar cortical infarct cavities are seen on MRI in as much as one third of patients with recently symptomatic vertebral artery stenosis. Since patients usually have no prior history of vertebrobasilar TIA or stroke, cerebellar cortical infarct cavities should be added to the spectrum of common incidental brain infarcts visible on routine MRI. (orig.)

Proposal for a universal definition of cerebral infarction.

Science.gov (United States)

Saver, Jeffrey L

2008-11-01

Cerebral infarction is a leading cause of disability and death worldwide but has no uniform international definition. Recent diagnostic advances have revised fundamental concepts in cerebral and cardiac ischemia. Cardiologists, already possessed of a nosologic framework distinguishing myocardial infarction from unstable angina on the basis of tissue state, promulgated a new "universal" tissue definition of myocardial infarction incorporating insights afforded by assays of cardiac troponin, a serum biomarker exquisitely sensitive to myocardial injury. Concurrently, vascular neurologists proposed a new tissue, rather than time, criterion to distinguish transient ischemia attack from cerebral infarction, responding to perspectives provided by diffusion MRI and cerebral blood volume CT, imaging biomarkers highly sensitive to neuronal injury. To complete this conceptual realignment, vascular neurology must now advance a clear, uniform, and operationalizable tissue definition of cerebral infarction. This review proposes cerebral infarction be defined as brain or retinal cell death due to prolonged ischemia. This definition categorizes both pannecrosis and neuronal dropout ("complete" and "incomplete" infarcts in classic neuropathologic terminology) as cerebral infarcts. Making the presence of any neuronal or glial cell death essential yields a definition of cerebral infarction that has high relevance to patients, physicians, and policymakers; is more easily applied in clinical practice; fosters action in acute care; harmonizes with myocardial ischemia classification; and focuses diagnostic evaluation on the cause of brain ischemia and the occurrence of end organ injury. The term cerebral infarction should be used when there is evidence of brain or retinal cell death due to cerebral ischemia.

Surgical outcome after decompressive craniectomy in patients with extensive cerebral infarction

International Nuclear Information System (INIS)

Otani, Naoki; Takasato, Yoshio; Masaoka, Hiroyuki

2008-01-01

Extensive cerebral hemispheric infarction is a devastating condition leading to early death in nearly 80% of cases due to the rapid rise of intracranial pressure in spite of maximum medical treatment for brain edema and swelling. Recently, decompressive craniectomy has been reevaluated to prevent the brain herniation caused by extensive hemispheric cerebral infarction. We studied the surgical results after decompressive craniectomy for extensive cerebral infarction. Between December 1997 and August 2006, 13 consecutive patients (7 males and 6 females aged from 39 to 73 with a mean age of 59 years) with massive cerebral infarction of internal carotid (IC) (11 patients) and middle cerebral artery (MCA) (2 patients) territory were treated with decompressive craniectomy and dural plasty. Five patients had a left-sided stroke with severe aphasia. The cardioembolic source of stroke was seen in 5 patients. Surgery was performed at the point of neurological deterioration, anisocoria, and effacement of perimesencephalic cistern on CT findings. The mean time between stroke onset and surgery was 39.8 hr and ranged from 13 to 102 hr. Glasgow outcome scale (GOS) on discharge was moderately disabled (MD) 1, severe disabled (SD) 5, vegetative state (VS) 1, and dead (D) 3 (mortality rate 30.8%). Severe pneumoniae were the causes of death. All survivors underwent cranioplasty and were transferred with the aim of rehabilitation. In this study, we showed that the decompressive craniectomy reduced mortality after extensive cerebral infarction. However, the functional outcome and level of independence are poor. It seems that the early decompressive craniectomy should be aggressively performed for extensive cerebral infarction before neurological deterioration such as worsening of consciousness disturbance or pupil abnormalities. Further investigations will be needed to clarify the surgical indications, timing, and functional outcomes. (author)

Atorvastatin therapy during the peri-infarct period attenuates left ventricular dysfunction and remodeling after myocardial infarction.

Directory of Open Access Journals (Sweden)

Xian-Liang Tang

Full Text Available Although statins impart a number of cardiovascular benefits, whether statin therapy during the peri-infarct period improves subsequent myocardial structure and function remains unclear. Thus, we evaluated the effects of atorvastatin on cardiac function, remodeling, fibrosis, and apoptosis after myocardial infarction (MI. Two groups of rats were subjected to permanent coronary occlusion. Group II (n = 14 received oral atorvastatin (10 mg/kg/d daily for 3 wk before and 4 wk after MI, while group I (n = 12 received equivalent doses of vehicle. Infarct size (Masson's trichrome-stained sections was similar in both groups. Compared with group I, echocardiographic left ventricular ejection fraction (LVEF and fractional area change (FAC were higher while LV end-diastolic volume (LVEDV and LV end-systolic and end-diastolic diameters (LVESD and LVEDD were lower in treated rats. Hemodynamically, atorvastatin-treated rats exhibited significantly higher dP/dt(max, end-systolic elastance (Ees, and preload recruitable stroke work (PRSW and lower LV end-diastolic pressure (LVEDP. Morphometrically, infarct wall thickness was greater in treated rats. The improvement of LV function by atorvastatin was associated with a decrease in hydroxyproline content and in the number of apoptotic cardiomyocyte nuclei. We conclude that atorvastatin therapy during the peri-infarct period significantly improves LV function and limits adverse LV remodeling following MI independent of a reduction in infarct size. These salubrious effects may be due in part to a decrease in myocardial fibrosis and apoptosis.

Impairment of Fos protein formation in the rat infarct borderzone by MK-801, but not by NBQX

DEFF Research Database (Denmark)

Christensen, Thomas; Jørgensen, M B; Diemer, Nils Henrik

1993-01-01

or a glutamate receptor antagonist; the non-competitive NMDA receptor antagonist MK-801 or the AMPA receptor antagonist NBQX which are known to be able to reduce infarct size in MCA occluded rats. The saline treated rats showed presence of Fos protein in nerve cell nuclei throughout the cortical and striatal...... infarct borderzone, but no staining in the infarct core or contralateral hemisphere. MK-801 almost totally abolished this expression of Fos protein whereas NBQX had no significant effect on Fos protein expression. It is suggested that the Fos protein induction is due to repeated spreading depressions...

Clinical estimation of myocardial infarct volume with MR imaging

International Nuclear Information System (INIS)

Johns, J.A.; Leavitt, M.B.; Field, B.D.; Yasuda, T.; Gold, H.; Leinbach, R.C.; Brady, T.J.; Dinsmore, R.E.

1987-01-01

MR imaging has not previously been used to assess infarct size in humans. Short-axis spin-echo cardiac MR imaging was performed in 20 patients who had undergone intravenous thrombolytic therapy and angiography, 10 days after myocardial infarct. A semi-automated computer program was used to outline the infarct region on each section. The outlines were algorithmically stacked and a three-dimensional representation of the infarct was created. The MR imaging infarct volume was then computed using the Simpson rule. Comparison with ventriculographic infarct size as determined by the computed severely hypokinetic segment length showed excellent correlation (r = .84, P < .001)

Ondine's Curse in a Patient with Unilateral Medullary and Bilateral Cerebellar Infarctions

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Hui-Tzu Ho

2005-11-01

Full Text Available Central sleep apnea (CSA, also known as Ondine's curse (OC, is a phenomenon characterized by episodes of repeated apnea during sleep due to disorders of the central nervous system. We report a patient with CSA/OC due to right dorsolateral medullary and bilateral cerebellar infarctions that occurred in the clinical setting of right vertebral artery stenosis. Polysomnography (PSG showed repeated episodes of absence of nasal cannula flow accompanying cessation of thoracic and abdominal respiratory movements and a decline in blood oxygen saturation. The duration of apnea was as long as 12 seconds. Brain magnetic resonance (MR images showed acute infarctions involving the right dorsolateral medulla, bilateral cerebellar vermis and paramedian cerebellar hemispheres. MR angiography showed nonvisualization of the right vertebral artery. Transcranial Doppler sonography showed a high resistance flow profile in the right vertebral artery and normal flow patterns in the basilar artery and left vertebral artery. These findings suggest that the medullary and bilateral cerebellar infarcts were caused by stenosis/pseudo-occlusion of the right vertebral artery. Reduced respiratory afferent inputs to the dorsal respiratory group of medullary neurons, the nucleus tractus solitarius and reduced “automatic” components of the respiratory drive may play a role in the development of CSA/OC.

Sgarbossa criteria and acute myocardial infarction.

Science.gov (United States)

Alang, Neha; Bathina, Jaya; Kranis, Mark; Angelis, Dimitrios

2010-01-01

Diagnosis of acute ST-elevation myocardial infarction in the presence of left bundle branch block is difficult. present a case of acute myocardial infarction with LBBB diagnosed and treated using the Sgarbossa criteria.

CT fogging effect with ischemic cerebral infarcts

International Nuclear Information System (INIS)

Becker, H.; Desch, H.; Hacker, H.; Pencz, A.; Frankfurt Univ.

1979-01-01

Systematic CT studies on ten patients with persistent ischemic cerebral infarct revealed a constant phenomenon, the fogging effect. The hypodense infarct at the beginning will be isodense, or close to isodense, on the plain CT during the second or third week and at a later stage will be hypodense again. The fogging infarcted area shows homogeneous intensive contrast enhancement. Knowledge of the fogging effect is important for correct interpretation of the CT image and the indication for contrast medium CT. CT without contrast medium may lead to misinterpretation during the second and third week after the onset of cerebral infarction. (orig.) [de

CT fogging effect with ischemic cerebral infarcts

Energy Technology Data Exchange (ETDEWEB)

Becker, H; Desch, H; Hacker, H; Pencz, A [Frankfurt Univ. (Germany, F.R.). Abt. fuer Neurologie; Frankfurt Univ. (Germany, F.R.). Abt. fuer Neuroradiologie)

1979-01-01

Systematic CT studies on ten patients with persistent ischemic cerebral infarct revealed a constant phenomenon, the fogging effect. The hypodense infarct at the beginning will be isodense, or close to isodense, on the plain CT during the second or third week and at a later stage will be hypodense again. The fogging infarcted area shows homogeneous intensive contrast enhancement. Knowledge of the fogging effect is important for correct interpretation of the CT image and the indication for contrast medium CT. CT without contrast medium may lead to misinterpretation during the second and third week after the onset of cerebral infarction.

Effects of Edaravone, a Free Radical Scavenger, on Photochemically Induced Cerebral Infarction in a Rat Hemiplegic Model

Directory of Open Access Journals (Sweden)

Satoshi Ikeda

2013-01-01

Full Text Available Edaravone is a free radical scavenger that protects the adjacent cortex during cerebral infarction. We created a hemiparetic model of cerebral thrombosis from a photochemically induced infarction with the photosensitive dye, rose bengal, in rats. We examined the effects of edaravone on recovery in the model. A total of 36 adult Wistar rats were used. The right sensorimotor area was irradiated with green light with a wavelength of 533 nm (10 mm diameter, and the rose bengal was injected intravenously to create an infarction. The edaravone group was injected intraperitoneally with edaravone (3 mg/kg, and the control group was injected with saline. The recovery process of the hemiplegia was evaluated with the 7-step scale of Fenny. The infarcted areas were measured after fixation. The recovery of the paralysis in the edaravone-treated group was significantly earlier than that in the untreated group. Seven days later, both groups were mostly recovered and had scores of 7, and the infarction region was significantly smaller in the edaravone-treated group. Edaravone reduced the infarction area and promoted the functional recovery of hemiparesis from cerebral thrombosis in a rat model. These findings suggest that edaravone treatment would be effective in clinical patients recovering from cerebral infarction.

Effects of edaravone, a free radical scavenger, on photochemically induced cerebral infarction in a rat hemiplegic model.

Science.gov (United States)

Ikeda, Satoshi; Harada, Katsuhiro; Ohwatashi, Akihiko; Kamikawa, Yurie

2013-01-01

Edaravone is a free radical scavenger that protects the adjacent cortex during cerebral infarction. We created a hemiparetic model of cerebral thrombosis from a photochemically induced infarction with the photosensitive dye, rose bengal, in rats. We examined the effects of edaravone on recovery in the model. A total of 36 adult Wistar rats were used. The right sensorimotor area was irradiated with green light with a wavelength of 533 nm (10 mm diameter), and the rose bengal was injected intravenously to create an infarction. The edaravone group was injected intraperitoneally with edaravone (3 mg/kg), and the control group was injected with saline. The recovery process of the hemiplegia was evaluated with the 7-step scale of Fenny. The infarcted areas were measured after fixation. The recovery of the paralysis in the edaravone-treated group was significantly earlier than that in the untreated group. Seven days later, both groups were mostly recovered and had scores of 7, and the infarction region was significantly smaller in the edaravone-treated group. Edaravone reduced the infarction area and promoted the functional recovery of hemiparesis from cerebral thrombosis in a rat model. These findings suggest that edaravone treatment would be effective in clinical patients recovering from cerebral infarction.

Influence of left ventricular hypertrophy on infarct size and left ventricular ejection fraction in ST-elevation myocardial infarction

International Nuclear Information System (INIS)

Małek, Łukasz A.; Śpiewak, Mateusz; Kłopotowski, Mariusz; Petryka, Joanna; Mazurkiewicz, Łukasz; Kruk, Mariusz; Kępka, Cezary; Miśko, Jolanta; Rużyłło, Witold; Witkowski, Adam

2012-01-01

Background: Left ventricular hypertrophy (LVH) predisposes to larger infarct size, which may be underestimated by the left ventricular ejection fraction (LVEF) due to supranormal systolic performance often present in patients with LVH. The aim of the study was to compare infarct size and LVEF in patients with ST-segment elevation myocardial infarction (STEMI) and increased left ventricular mass on cardiac magnetic resonance (CMR). Methods: The study included unselected group of 52 patients (61 ± 11 years, 69% male) with first STEMI who had CMR after median 5 days from the onset of the event. Left ventricular hypertrophy (LVH) was defined as left ventricular mass index exceeding 95th percentile of references values for age and gender. Infarct size was assessed with means of late gadolinium enhancement (LGE). Results: LVH was found in 16 patients (31%). In comparison to the rest of the group, patients with LVH had higher absolute and relative infarct mass (p = 0.002 and p = 0.02, respectively). LVH was related to higher prevalence of microvascular obstruction and myocardial haemorrhage and higher number of LV segments with transmural necrosis (p = 0.02, p = 0.01 and p = 0.01, respectively). Despite marked difference in the infarct size between both studied subgroups there was no difference in LVEF and mean number of dysfunctional LV segments. Conclusions: Patients with LVH undergoing STEMI have larger infarct size underestimated by the LV systolic performance in comparison to patients without LVH.

Spontaneous Hepatic Infarction in a Patient with Gallbladder Cancer

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Kang Min Lee

2016-06-01

Full Text Available Hepatic infarction is known as a rare disease entity in nontransplant patients. Although a few cases of hepatic infarction have been reported to be linked with invasive procedures, trauma, and hypercoagulability, a case of spontaneous hepatic infarction in a nontransplanted patient has hardly ever been reported. However, many clinical situations of patients with cancer, in particular biliary cancer, can predispose nontransplant patients to hepatic infarction. Besides, the clinical outcome of hepatic infarction in patients with cancer can be worse than in patients with other etiologies. As for treatment, anticoagulation treatment is usually recommended. However, because of its multifactorial etiology and combined complications, treatment of hepatic infarction is difficult and not simple. Herein, we report a case of fatal hepatic infarction that occurred spontaneously during the course of treatment in a patient with gallbladder cancer. Hepatic infarction should be considered as a possible fatal complication in patients during treatment of biliary malignancies.

Diffusion-weighted echo-planar MRI of lacunar infarcts

International Nuclear Information System (INIS)

Noguchi, K.; Nagayoshi, T.; Watanabe, N.; Kanazawa, T.; Toyoshima, S.; Morijiri, M.; Shojaku, H.; Shimizu, M.; Seto, H.

1998-01-01

We studied 35 patients with lacunar infarcts, using diffusion-weighted echo-planar imaging (DW-EPI) at 1.5 T. The relative apparent diffusion coefficient ratio (ADCR) of each lesion was calculated and lesion conspicuity on DW-EPI was compared to that on images aquired with fast fluid-attenuated inversion recovery and T2-weighted fast spin-echo sequences. Acute small infarcts (within 3 days) were identified with DW-EPI as an area of decreased ADCR (range 0.33-0.87; mean 0.67) and high signal, subacute small infarcts (4-30 days) as a high-signal or isointense areas of decreased or nearly normal ADCR (0.54-0.98; 0.73), and chronic small infarcts (> 30 days) as low- or high-signal areas of nearly normal or increased ADCR (0.97-1.92; 1.32). In three patients, small infarcts of the brain stem in the hyperacute phase (within 6 h) were seen only with DW-EPI. In five patients, fresh small infarcts adjacent to multiple old infarcts could be distinguished only with DW-EPI. (orig.)

System delay and timing of intervention in acute myocardial infarction (from the Danish Acute Myocardial Infarction-2 [DANAMI-2] trial)

DEFF Research Database (Denmark)

Nielsen, Peter Haubjerg; Terkelsen, Christian Juhl; Nielsen, Torsten Toftegård

2011-01-01

The interval from the first alert of the healthcare system to the initiation of reperfusion therapy (system delay) is associated with mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention (pPCI). The importance of system delay...... in patients treated with fibrinolysis versus pPCI has not been assessed. We obtained data on system delay from the Danish Acute Myocardial Infarction-2 study, which randomized 1,572 patients to fibrinolysis or pPCI. The study end points were 30-day and 8-year mortality. The short system delays were associated...... with reduced absolute mortality in both the fibrinolysis group (3 hours, 11.5%; test for trend, p = 0.08) and pPCI group (3 hours, 7.7%; test for trend, p = 0.02). The lowest 30-day mortality was obtained with pPCI and a system delay of 1 to 2 hours (vs fibrinolysis within 3 hours was associated with a similar...

Hemicraniectomy after middle cerebral artery infarction with life-threatening Edema trial (HAMLET). Protocol for a randomised controlled trial of decompressive surgery in space-occupying hemispheric infarction.

Science.gov (United States)

Hofmeijer, Jeannette; Amelink, G Johan; Algra, Ale; van Gijn, Jan; Macleod, Malcolm R; Kappelle, L Jaap; van der Worp, H Bart

2006-09-11

Patients with a hemispheric infarct and massive space-occupying brain oedema have a poor prognosis. Despite maximal conservative treatment, the case fatality rate may be as high as 80%, and most survivors are left severely disabled. Non-randomised studies suggest that decompressive surgery reduces mortality substantially and improves functional outcome of survivors. This study is designed to compare the efficacy of decompressive surgery to improve functional outcome with that of conservative treatment in patients with space-occupying supratentorial infarction The study design is that of a multi-centre, randomised clinical trial, which will include 112 patients aged between 18 and 60 years with a large hemispheric infarct with space-occupying oedema that leads to a decrease in consciousness. Patients will be randomised to receive either decompressive surgery in combination with medical treatment or best medical treatment alone. Randomisation will be stratified for the intended mode of conservative treatment (intensive care or stroke unit care). The primary outcome measure will be functional outcome, as determined by the score on the modified Rankin Scale, at one year.

Spectral analysis of epicardial 60-lead electrograms in dogs with 4-week-old myocardial infarction.

Science.gov (United States)

Hosoya, Y; Ikeda, K; Komatsu, T; Yamaki, M; Kubota, I

2001-01-01

There were few studies on the spectral analysis of multiple-lead epicardial electrograms in chronic myocardial infarction. Spectral analysis of multi-lead epicardial electrograms was performed in 6 sham-operated dogs (N group) and 8 dogs with 4-week-old myocardial infarction (MI group). Four weeks after the ligation of left anterior descending coronary artery, fast Fourier transform was performed on 60-lead epicardial electrograms, and then inverse transform was performed on 5 frequency ranges from 0 to 250 Hz. From the QRS onset to QRS offset, the time integration of unsigned value of reconstructed waveform was calculated and displayed as AQRS maps. On 0-25 Hz AQRS map, there was no significant difference between the 2 groups. In the frequency ranges of 25-250 Hz, MI group had significantly smaller AQRS values than N group solely in the infarct zone. It was shown that high frequency potentials (25-250 Hz) within QRS complex were reduced in the infarct zone.

Laser microdissection and capture of pure cardiomyocytes and fibroblasts from infarcted heart regions: perceived hyperoxia induces p21 in peri-infarct myocytes.

Science.gov (United States)

Kuhn, Donald E; Roy, Sashwati; Radtke, Jared; Khanna, Savita; Sen, Chandan K

2007-03-01

Myocardial infarction caused by ischemia-reperfusion in the coronary vasculature is a focal event characterized by an infarct-core, bordering peri-infarct zone and remote noninfarct zone. Recently, we have reported the first technique, based on laser microdissection pressure catapulting (LMPC), enabling the dissection of infarction-induced biological responses in multicellular regions of the heart. Molecular mechanisms in play at the peri-infarct zone are central to myocardial healing. At the infarct site, myocytes are more sensitive to insult than robust fibroblasts. Understanding of cell-specific responses in the said zones is therefore critical. In this work, we describe the first technique to collect the myocardial tissue with a single-cell resolution. The infarcted myocardium was identified by using a truncated hematoxylin-eosin stain. Cell elements from the infarct, peri-infarct, and noninfarct zones were collected in a chaotropic RNA lysis solution with micron-level surgical precision. Isolated RNA was analyzed for quality by employing microfluidics technology and reverse transcribed to generate cDNA. Purity of the collected specimen was established by real-time PCR analyses of cell-specific genes. Previously, we have reported that the oxygen-sensitive induction of p21/Cip1/Waf1/Sdi1 in cardiac fibroblasts in the peri-infarct zone plays a vital role in myocardial remodeling. Using the novel LMPC technique developed herein, we confirmed that finding and report for the first time that the induction of p21 in the peri-infarct zone is not limited to fibroblasts but is also evident in myocytes. This work presents the first account of an analytical technique that applies the LMPC technology to study myocardial remodeling with a cell-type specific resolution.

Myocardial infarction, androgen and the skin.

Science.gov (United States)

Halim, M M; Meyrick, G; Jeans, W D; Murphy, D; Burton, J L

1978-01-01

Various indices of masculinity were compared in 48 men who had recovered from myocardial infarction and in their age-matched controls. We found little evidence to support the idea that myocardial infarction is related to increased androgenic stimulation. The patients with myocardial infarction had no increase in plasma testosterone, muscle thickness, sebum excretion rate, maximal sweat secretion rate, male pattern alopecia or density of terminal body hair, but as a group they had a slight increase in skin and bone thickness compared with the controls.

Is the time between onset of pain and restoration of patency of infarct-related artery shortened in patients with myocardial infarction? The effects of the Kielce Region System for Optimal Management of Acute Myocardial Infarction

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Marcin Sadowski

2014-09-01

Full Text Available Introduction : The importance of delay in the restoration of infarct-related artery patency in patients with myocardial infarction was discussed, and actions were undertaken in the Kielce Region aimed at shortening this time within the System for Optimal Management of Acute Myocardial Infarction. Aim of the research: To evaluate the effectiveness of shortening time delays during transport of patients and diagnostics of myocardial infarction in the Kielce Region. Material and methods: Time delays were analysed in 5,934 patients with ST-segment elevation myocardial infarction (STEMI, hospitalised in cardiology wards with interventional cardiology on 24-hour duty, during the period 2008–2012. Time delays were analysed between the onset of myocardial infarction pain and undertaking treatment – T1 and T2 time – within which a patient with myocardial infarction, after admission to hospital, has intervention performed on infarct-related coronary artery. Results : During the period 2008–2012, the median T1 time was successfully shortened from 355 to 203 min, and the T2 time from 101 to 48 min. Conclusions: The effectiveness of the system was confirmed, and the necessity for further improvement of the system indicated.

Computerized detection of lacunar infarcts in brain MR images

International Nuclear Information System (INIS)

Uchiyama, Yoshikazu; Matsui, Atsushi; Yokoyama, Ryujiro

2007-01-01

Asymptomatic lacunar infarcts are often found in the Brain Dock. The presence of asymptomatic lacunar infarcts increases the risk of serious cerebral infarction. Thus, it is an important task for radiologists and/or neurosurgeons to detect asymptomatic lacunar infarctions in MRI images. However, it is difficult for radiologists and/or neurosurgeons to identify lacunar infarcts correctly in MRI images, because it is hard to distinguish between lacunar infarcts and enlarged Virchow-Robin space. Therefore, the purpose of our study was to develop a computer-aided diagnosis scheme for detection of lacunar infarctions in order to assist radiologists and/or neurosurgeons' interpretation as a ''second opinion.'' Our database consisted of 1143 T2-weighted MR images and 1143 T1-weighted MR images, which were selected from 132 patients. First, we segmented the cerebral parenchyma region by use of a region growing technique. The white-tophat transformation was then applied for enhancement of lacunar infarcts. The multiple-phase binarization was used for identifying initial candidates of lacunar infarcts. For removal of false positives (FPs), 12 features were determined in each of the initial candidates in T2 and T1-weighted MR images. The rule-based schemes and an artificial neural network with these features were used for distinguishing between lacunar infarcts and FPs. The sensitivity of detection of lacunar infarcts was 96.8% (90/93) with 0.69 (737/1063) FP per image. This computerized method may be useful for radiologists and/or neurosurgeons in detecting lacunar infracts in MRI images. (author)

Contrast MR imaging of acute cerebral infarction

Energy Technology Data Exchange (ETDEWEB)

Kogame, Saeko; Syakudo, Miyuki; Inoue, Yuichi (Osaka City Univ. (Japan). Faculty of Medicine) (and others)

1992-04-01

Thirty patients with acute and subacute cerebral infarction (13 and 17 deep cerebral infarction) were studied with 0.5 T MR unit before and after intravenous injection of Gd-DTPA. Thirteen patients were studied within 7 days after neurological ictus, 17 patients were studied between 7 and 14 days. Two types of abnormal enhancement, cortical arterial and parenchymal enhancement, were noted. The former was seen in 3 of 4 cases of very acute cortical infarction within 4 days after clinical ictus. The latter was detected in all 7 cases of cortical infarction after the 6th day of the ictus, and one patient with deep cerebral infarction at the 12th day of the ictus. Gd-DTPA enhanced MR imaging seems to detect gyral enhancement earlier compared with contrast CT, and depict intra-arterial sluggish flow which was not expected to see on contrast CT scans. (author).

Dynamic CT scan in cerebral infarction

International Nuclear Information System (INIS)

Kobayashi, Shigeki; Oka, Nobuo; Mitsuhashi, Hiromitsu

1984-01-01

Forty-two dynamic CT studies were performed on 27 patients with cerebral infarction (11 to 75 years of age), and perfusion patterns of low density areas on plain CT were evaluated. The initial studies were performed 1.5 hours to 60 days after acute onset. The following results were obtained. 1) The perfusion pattern in the low density area on plain CT varies among patients at any periods after onset, ranging from absent perfusion pattern to hyperfusion pattern. No consisitent perfusion pattern was obtained at any given time after onset. 2) Repeat dynamic CT revealed that the perfusion pattern in the low density area changed with time variously. 3) The perfusion pattern or change of perfusion pattern did not correlate with outcome of the patient. 4) At an acute stage, when no abnormal findings were obtained on plain CT, dynamic CT revealed abnormal perfusion pattern, enabling early diagnosis of cerebral infarction and estimation of blood perfusion in the infarcted area. In determining the treatment for the cerebral infarction at an acute stage, it is important to know the condition of the blood perfusion in the infarcted area. For the patients in whom recanalization has already taken place, mannitol or steroid might be effective, providing protection against severe brain edema and hemorrhagic infarction. On the other hand, if recanalization has not taken place, revascularization therapy might be worth trying within 6 hours since the onset. It has been said that ischemic brain damage may not be reversed by the revascularization after 6 hours. Dynamic CT is safe, less invasive, convenient and very useful for early diagnosis of the cerebral infarction and determination of the treatment at the acute stage. (J.P.N.)

Short-term fasting reduces the extent of myocardial infarction and incidence of reperfusion arrhythmias in rats

Czech Academy of Sciences Publication Activity Database

Šnorek, M.; Hodyc, D.; Šedivý, V.; Ďurišová, J.; Skoumalová, A.; Wilhelm, J.; Neckář, Jan; Kolář, František; Herget, J.

2012-01-01

Roč. 61, č. 6 (2012), s. 567-574 ISSN 0862-8408 R&D Projects: GA MŠk(CZ) 1M0510; GA ČR(CZ) GA305/08/0108 Institutional research plan: CEZ:AV0Z5011922 Keywords : myocardial ischemia/reperfusion * arrhythmias * infarction * fasting * ketone bodies Subject RIV: FA - Cardiovascular Diseases incl. Cardiotharic Surgery Impact factor: 1.531, year: 2012

Locations of cerebral infarctions in tuberculous meningitis

International Nuclear Information System (INIS)

Hsieh, F.Y.; Chia, L.G.; Shen, W.C.

1992-01-01

The locations of cerebral infarctions were studied in 14 patients with tuberculous meningitis (TBM) and 173 patients with noninflammatory ischemic stroke (IS). In patients with TBM, 75% of infarctions occurred in the 'TB zone' supplied by medial striate and thalamoperforating arteries; only 11% occurred in the 'IS zone' supplied by lateral striate, anterior choroidal and thalamogeniculate arteries. In patients with IS, 29% of infarctions occurred in the IS zone, 29% in the subcortical white matter, and 24% in (or involving) the cerebral cortex. Only 11% occurred in the TB zone. Bilaterally symmetrical infarctions of the TB zone were common with TBM (71%) but rare with IS (5%). (orig.)

Myocardial infarction in Swedish subway drivers.

Science.gov (United States)

Bigert, Carolina; Klerdal, Kristina; Hammar, Niklas; Gustavsson, Per

2007-08-01

Particulate matter in urban air is associated with the risk of myocardial infarction in the general population. Very high levels of airborne particles have been detected in the subway system of Stockholm, as well as in several other large cities. This situation has caused concern for negative health effects among subway staff. The aim of this study was to investigate whether there is an increased incidence of myocardial infarction among subway drivers. Data from a population-based case-control study of men aged 40-69 in Stockholm County in 1976-1996 were used. The study included all first events of myocardial infarction in registers of hospital discharges and deaths. The controls were selected randomly from the general population. National censuses were used for information on occupation. Altogether, 22 311 cases and 131 496 controls were included. Among these, 54 cases and 250 controls had worked as subway drivers. The relative risk of myocardial infarction among subway drivers was not increased. It was 0.92 [95% confidence interval (95% CI) 0.68-1.25] when the subway drivers were compared with other manual workers and 1.06 (95% CI 0.78-1.43) when the subway drivers were compared with all other gainfully employed men. Subgroup analyses indicated no influence on the risk of myocardial infarction from the duration of employment, latency time, or time since employment stopped. Subway drivers in Stockholm do not have a higher incidence of myocardial infarction than other employed persons.

The relationship between ECG signs of atrial infarction and the development of supraventricular arrhythmias in patients with acute myocardial infarction

DEFF Research Database (Denmark)

Nielsen, F E; Andersen, H H; Gram-Hansen, P

1992-01-01

ECGs obtained on arrival at the hospital from 277 patients with acute myocardial infarction were analyzed retrospectively for PR displacements, which were classified as major or minor criteria for atrial infarction and related to the later occurrence of supraventricular arrhythmia in the hospital...... arrhythmias, giving odds ratios of 9.9 and 3.7, respectively. Enzyme-estimated infarct size, the occurrence of heart failure, and mortality rates did not differ in patients with or without major criteria for atrial infarction. We conclude that the occurrence of PR segment displacements on the admission ECG...

Quantitative estimation of viable myocardium in the infarcted zone by infarct-redistribution map from images of exercise thallium-201 emission computed tomography

International Nuclear Information System (INIS)

Sekiai, Yasuhiro

1988-01-01

To evaluate, quantitatively, the viable myocardium in the infarcted zone, we invented the infarct-redistribution map which is produced from images of exercise thallium-201 emission computed tomography performed on 10 healthy subjects and 20 patients with myocardial infarction. The map displayed a left ventricle in which the infarcted area both with and without redistribution, the redistribution area without infarction, and normal perfusion area were shown separated in same screen. In these circumstances, the nonredistribution infarct lesion was found as being surrounded by the redistribution area. Indices of infarct and redistribution extent (defect score, % defect, redistribution ratio (RR) and redistribution index (RI)), were induced from the map and were used for quantitative analysis of the redistribution area and as the basis for comparative discussion regarding regional wall motion of the left ventricle. The quantitative indices of defect score, % defect, RR and RI were consistent with the visual assessment of planar images in detecting the extent of redistribution. Furthermore, defect score and % defect had an inverted linear relationship with % shortening (r = -0.573; p < 0.05, r = -0.536; p < 0.05, respectively), and RI had a good linear relationship with % shortening (r = 0.669; p < 0.01). We conclude that the infarct-redistribution map accurately reflects the myocardial viability and therefore may be useful for quantitative estimation of viable myocardium in the infarcted zone. (author)

Quantitative Assessment of Myocardial Infarction by In-111 Antimyosin Antibody

Energy Technology Data Exchange (ETDEWEB)

Lee, Myung Chul; Lee, Kyung Han; Choi, Yoon Ho; Chung, June Key; Park, Young Bae; Koh, Chang Soon [Seoul National University College of Medicine, Seoul (Korea, Republic of); Moon, Dae Hyuk [Asan Medical Center, Ulsan University College of Medicine, Seoul (Korea, Republic of)

1991-03-15

Infarct size is a major determinant of prognosis after acute myocardial infarction. Up to date, however, clinically available tests to estimate this size have not been sufficiently accurate. Twelve lead electrocardiogram and wall motion abnormality measurement are not quantitative, and creatine phosphokinase (CPK) measurement is inaccurate in the presence of reperfusion or right ventricular infarction. Methods have been developed to localize and size acute myocardial infarcts with agents that are selectively sequestered in areas of myocardial damage, but previously used agents have lacked sufficient specificity. Antibodies that bind specifically only to damaged myocardial cells may resolve this problem and provide an accurate method for noninvasively measuring infarct size. We determined the accuracy with which infarcted myocardial mass can be measured using single photon emission computed tomography (SPECT) and radiolabeled antimyosin antibodies. Seven patients with acute myocardial infarction and one stable angina patient were injected with 2 mCi of Indium-111 labeled antimyosin antibodies. Planar image and SPECT was performed 24 hours later. None of the patients had history of prior infarcts, and none had undergone reperfusion techniques prior to the study, which was done within 4 days of the attack. Planar image showed all infarct patients to have positive uptakes in the cardiac region. The location of this uptake correlated to the infarct site as indicated by electrocardiography in most of the cases. The angina patient, however, showed no such abnormal uptake. Infarct size was determined from transverse slices of the SPECT image using a 45% threshold value obtained from a phantom study. Measured infarct size ranged from 40 to 192 gr. There was significant correlation between the infarct size measured by SPECT and that estimated from serial measurements of CPK (r=0.73, p<0,05). These date suggest that acute myocardial infarct size can be accurately measured

Practical guidelines for treatment with beta-blockers and nitrates in patients with acute myocardial infarction

NARCIS (Netherlands)

M.L. Simoons (Maarten); P.W.J.C. Serruys (Patrick); P.M. Fioretti (Paolo); M.J.B.M. van den Brand (Marcel); P.G. Hugenholtz (Paul)

1983-01-01

textabstractTreatment of a patient with myocardial infarction might include opiates and sedatives to reduce pain and anxiety, heparin, antiarrhythmic drugs, diuretics which aim at improvement of myocardial function and drugs which might reduce the ischemic area at risk and thus mortality such as

Effects on infarct size and left ventricular function of early intravenous injection of anistreplase in acute myocardial infarction. The APSIM Study Investigators.

Science.gov (United States)

Bassand, J P; Bernard, Y; Lusson, J R; Machecourt, J; Cassagnes, J; Borel, E

1990-03-01

A total of 231 patients suffering from a first acute myocardial infarction were randomly allocated within 4 hours following the onset of symptoms either to anistreplase or anisoylated plasminogen streptokinase activator complex (APSAC), 30 U over 5 minutes, or to conventional heparin therapy, 5000 IU in bolus injection. Heparin was reintroduced in both groups 4 h after initial therapy at a dosage of 500 IU/kg per day. A total of 112 patients received anistreplase and 119 received heparin within a mean period of 188 +/- 62 min following the onset of symptoms. Infarct size was estimated from single photon emission computerized tomography and expressed in percentage of the total myocardial volume. The patency rate of the infarct-related artery was 77% in the anistreplase group and 36% in the heparin group (p less than 0.001). Left ventricular ejection fraction determined from contrast angiography was significantly higher in the anistreplase group than in the heparin group (6 absolute percentage point difference). A significant 31% reduction in infarct size was found in the anistreplase group (33% for the anterior wall infarction subgroup [p less than 0.05] and 16% for the inferior wall infarction subgroup, NS). A close inverse relation was found between the values of left ventricular ejection fraction and infarct size (r = -.73, p less than 0.01). In conclusion, early infusion of anistreplase in acute myocardial infarction produced a high early patency rate, a significant limitation of infarct size, and a significant preservation of left ventricular systolic function, mainly in the anterior wall infarctions.

Plasma HDL cholesterol and risk of myocardial infarction : A mendelian randomisation study

NARCIS (Netherlands)

Voight, Benjamin F.; Peloso, Gina M.; Orho-Melander, Marju; Frikke-Schmidt, Ruth; Barbalic, Maja; Jensen, Majken K.; Hindy, George; Holm, Hilma; Ding, Eric L.; Johnson, Toby; Schunkert, Heribert; Samani, Nilesh J.; Clarke, Robert; Hopewell, Jemma C.; Thompson, John F.; Li, Mingyao; Thorleifsson, Gudmar; Newton-Cheh, Christopher; Musunuru, Kiran; Pirruccello, James P.; Saleheen, Danish; Chen, Li; Stewart, Alexandre F. R.; Schillert, Arne; Thorsteinsdottir, Unnur; Thorgeirsson, Gudmundur; Anand, Sonia; Engert, James C.; Morgan, Thomas; Spertus, John; Stoll, Monika; Berger, Klaus; Martinelli, Nicola; Girelli, Domenico; McKeown, Pascal P.; Patterson, Christopher C.; Epstein, Stephen E.; Devaney, Joseph; Burnett, Mary-Susan; Mooser, Vincent; Ripatti, Samuli; Surakka, Ida; Nieminen, Markku S.; Sinisalo, Juha; Lokki, Marja-Liisa; Perola, Markus; Havulinna, Aki; de Faire, Ulf; Gigante, Bruna; Ingelsson, Erik; Zeller, Tanja; Wild, Philipp; de Bakker, Paul I. W.; Klungel, Olaf H.; Maitland-van der Zee, Anke-Hilse; Peters, Bas J. M.; de Boer, Anthonius; Grobbee, Diederick E.; Kamphuisen, Pieter W.; Deneer, Vera H. M.; Elbers, Clara C.; Onland-Moret, N. Charlotte; Hofker, Marten H.; Wijmenga, Cisca; Verschuren, W. M. Monique; Boer, Jolanda M. A.; van der Schouw, Yvonne T.; Rasheed, Asif; Frossard, Philippe; Demissie, Serkalem; Willer, Cristen; Do, Ron; Ordovas, Jose M.; Abecasis, Goncalo R.; Boehnke, Michael; Mohlke, Karen L.; Daly, Mark J.; Guiducci, Candace; Burtt, Noel P.; Surti, Aarti; Gonzalez, Elena; Purcell, Shaun; Gabriel, Stacey; Marrugat, Jaume; Peden, John; Erdmann, Jeanette; Diemert, Patrick; Willenborg, Christina; Koenig, Inke R.; Fischer, Marcus; Hengstenberg, Christian; Ziegler, Andreas; Buysschaert, Ian; Lambrechts, Diether; Van de Werf, Frans; Fox, Keith A.; El Mokhtari, Nour Eddine; Rubin, Diana; Schrezenmeir, Juergen; Schreiber, Stefan; Schaefer, Arne; Danesh, John; Blankenberg, Stefan; Roberts, Robert; McPherson, Ruth; Watkins, Hugh; Hall, Alistair S.; Overvad, Kim; Rimm, Eric; Boerwinkle, Eric; Tybjaerg-Hansen, Anne; Cupples, L. Adrienne; Reilly, Muredach P.; Melander, Olle; Mannucci, Pier M.; Ardissino, Diego; Siscovick, David; Elosua, Roberto; Stefansson, Kari; O'Donnell, Christopher J.; Salomaa, Veikko; Rader, Daniel J.; Peltonen, Leena; Schwartz, Stephen M.; Altshuler, David; Kathiresan, Sekar

2012-01-01

Background High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease

Relationship between blood uric and acute cerebral infarction

International Nuclear Information System (INIS)

Yin Zhanxia; Zhao Danyang

2011-01-01

Objective: To study the relationship between blood uric acid and acute cerebral infarction. Methods: The level of blood uric acid and prevalence of hyperuricemia (HUA) were compared in 360 patients with acute cerebral infarction and 300 patients without it. According to the level of blood uric acid, 360 acute cerebral infarction patients were divided into HUA and normouricemia (NUA) groups. Age, sex, body mass index (BMI), blood glucose and total cholesterol were compared between the HUA and NUA group. The degree of neurological functional defection was compared between the two groups when patients were attacked by acute cerebral infarction. After a recovery treatment, the neurological functional defection of the two groups was compared a second time. Results: (1)The average blood uric acid level and prevalence of HUA were higher in patients with acute cerebral infarction. (2) The BMI, blood glucose and total cholesterol were higher in HUA group than in NUA group. (3) The neurological functional defection was more serious in HUA group when patients were attacked by acute cerebral infarction and after a recovery treatment. Conclusion: Hyperuricemia is related to acute cerebral infarction. (authors)

Docosahexaenoic acid confers enduring neuroprotection in experimental stroke.

Science.gov (United States)

Hong, Sung-Ha; Belayev, Ludmila; Khoutorova, Larissa; Obenaus, Andre; Bazan, Nicolas G

2014-03-15

Recently we demonstrated that docosahexaenoic acid (DHA) is highly neuroprotective when animals were allowed to survive during one week. This study was conducted to establish whether the neuroprotection induced by DHA persists with chronic survival. Sprague-Dawley rats underwent 2h of middle cerebral artery occlusion (MCAo) and treated with DHA or saline at 3h after MCAo. Animals received neurobehavioral examination (composite neuroscore, rota-rod, beam walking and Y maze tests) followed by ex vivo magnetic resonance imaging and histopathology at 3 weeks. DHA improved composite neurologic score beginning on day 1 by 20%, which persisted throughout weeks 1-3 by 24-41% compared to the saline-treated group. DHA prolonged the latency in rota-rod on weeks 2-3 by 162-178%, enhanced balance performance in the beam walking test on weeks 1 and 2 by 42-51%, and decreased the number of entries in the Y maze test by 51% and spontaneous alteration by 53% on week 2 compared to the saline-treated group. DHA treatment reduced tissue loss (computed from T2-weighted images) by 24% and total and cortical infarct volumes by 46% and 54% compared to the saline-treated group. These results show that DHA confers enduring ischemic neuroprotection. Copyright © 2013 The Authors. Published by Elsevier B.V. All rights reserved.

Association of splenic and renal infarctions in acute abdominal emergencies

Energy Technology Data Exchange (ETDEWEB)

Romano, Stefania E-mail: stefromano@libero.it; Scaglione, Mariano; Gatta, Gianluca; Lombardo, Patrizia; Stavolo, Ciro; Romano, Luigia; Grassi, Roberto

2004-04-01

Introduction: Splenic and renal infarctions are usually related to vascular disease or haematologic abnormalities. Their association is infrequent and rarely observed in trauma. In this study, we analyze our data to look at the occurrence of renal and splenic infarctions based on CT findings in a period of 4 years. Materials and Methods: We retrospectively reviewed the imaging findings of 84 patients admitted to our Department of Diagnostic Imaging from June 1998 to December 2002, who underwent emergency abdominal spiral CT examination and in whom there was evidence of splenic and/or renal infarction. Results: We found 40 cases of splenic infarction and 54 cases of renal infarction, associated in 10 patients. In 26 patients, there was also evidence of intestinal infarction. A traumatic origin was found in 19 cases; non-traumatic causes were found in 65 patients. Association between renal and splenic infarction in the same patient was related to trauma in two cases. Conclusions: Although renal and splenic infarctions are a common manifestation of cardiac thromboembolism, other systemic pathologies, infections or trauma may lead to this occurrence. Renal infarction may be clinically and/or surgically managed with success in most cases. There are potential complications in splenic infarction, such as development of pseudocysts, abscesses, hemorrhage, subcapsular haematoma or splenic rupture; splenectomy in these cases may be necessary. Some patients with splenic and/or renal infarction may be clinically asymptomatic. The high accuracy of CT examination is needed to allow a correct evaluation of infarcted organs.

Association of splenic and renal infarctions in acute abdominal emergencies

International Nuclear Information System (INIS)

Romano, Stefania; Scaglione, Mariano; Gatta, Gianluca; Lombardo, Patrizia; Stavolo, Ciro; Romano, Luigia; Grassi, Roberto

2004-01-01

Introduction: Splenic and renal infarctions are usually related to vascular disease or haematologic abnormalities. Their association is infrequent and rarely observed in trauma. In this study, we analyze our data to look at the occurrence of renal and splenic infarctions based on CT findings in a period of 4 years. Materials and Methods: We retrospectively reviewed the imaging findings of 84 patients admitted to our Department of Diagnostic Imaging from June 1998 to December 2002, who underwent emergency abdominal spiral CT examination and in whom there was evidence of splenic and/or renal infarction. Results: We found 40 cases of splenic infarction and 54 cases of renal infarction, associated in 10 patients. In 26 patients, there was also evidence of intestinal infarction. A traumatic origin was found in 19 cases; non-traumatic causes were found in 65 patients. Association between renal and splenic infarction in the same patient was related to trauma in two cases. Conclusions: Although renal and splenic infarctions are a common manifestation of cardiac thromboembolism, other systemic pathologies, infections or trauma may lead to this occurrence. Renal infarction may be clinically and/or surgically managed with success in most cases. There are potential complications in splenic infarction, such as development of pseudocysts, abscesses, hemorrhage, subcapsular haematoma or splenic rupture; splenectomy in these cases may be necessary. Some patients with splenic and/or renal infarction may be clinically asymptomatic. The high accuracy of CT examination is needed to allow a correct evaluation of infarcted organs

Surgical dissection of the internal carotid artery under flow control by proximal vessel clamping reduces embolic infarcts during carotid endarterectomy.

Science.gov (United States)

Yoshida, Kazumichi; Kurosaki, Yoshitaka; Funaki, Takeshi; Kikuchi, Takayuki; Ishii, Akira; Takahashi, Jun C; Takagi, Yasushi; Yamagata, Sen; Miyamoto, Susumu

2014-01-01

To evaluate the efficacy of flow control of the internal carotid artery (ICA) by the clamping of the common carotid artery, external carotid artery, and superior thyroid artery during surgical ICA dissection to reduce ischemic complications after carotid endarterectomy (CEA). Sixty-seven patients (59 men; age, 70.5 ± 6.2 years) who underwent CEA by the same surgeon were retrospectively studied. Both conventional CEA (n = 29) and flow-control CEA (n = 38) were performed with the patient under general anesthesia and with the use of somatosensory-evoked potential and near-infrared spectroscopy monitoring as a guide for selective shunting. The number of new postoperative infarcts was assessed with preoperative and postoperative diffusion-weighted images (DWIs) obtained within 3 days of surgery. In addition to surgical technique, the effects of the following factors on new infarcts also were examined: age, side of ICA stenosis, high-grade stenosis, symptoms, and application of shunting. New postoperative DWI lesions were observed in 7 of 67 patients (10.4%), and none of them was symptomatic. With respect to operative technique, the incidence rate of DWI spots was significantly lower in the flow-control group (2.6%) than in the conventional group (20.7%), odds ratio: 0.069; 95% confidence interval: 0.006-0.779; P = 0.031). On multiple logistic regression analysis, age, side of ICA stenosis, high-grade stenosis, symptoms, and the use of internal shunting did not have significant effects on new postoperative DWI lesions, whereas technique did have an effect. The proximal flow-control technique for CEA helps avoid embolic complications during surgical ICA dissection. Copyright © 2014 Elsevier Inc. All rights reserved.

The post-pulmonary infarction syndrome.

Science.gov (United States)

Sklaroff, H J

1979-12-01

Following pulmonary infarction, three patients developed the classical signs and symptoms of the Dressler syndrome associated with persistent left pleural effusion. Each responded dramatically to corticosteroid therapy. While the pathogenesis of this "Post-Pulmonary Infarction syndrome," like the Dressler syndrome, is unclear, the response to corticosteroid therapy is both dramatic and diagnostic and may spare the patient prolonged discomfort and unnecessary diagnostic procedures.

Smoking Status and Incidence of Cancer After Myocardial Infarction: A Follow-Up Study of over 20 Years.

Science.gov (United States)

Lotan, Katrin; Goldbourt, Uri; Gerber, Yariv

2017-09-01

We evaluated long-term incidence of cancer after myocardial infarction among current, former, and never smokers, and assessed whether reducing cigarette consumption is associated with decreased cancer risk. Consecutive patients aged ≤65 years discharged from 8 hospitals in central Israel after first myocardial infarction in 1992-1993 were followed for cancer and death. Extensive data including smoking habits were obtained at the index hospitalization and 4 time points during follow-up. Survival methods were applied to assess the hazard ratios (HRs) for cancer associated with smoking categories. Included in the study were 1486 cancer-free participants (mean age, 54 years; 81% men), among whom 787 were current smokers at baseline (average daily cigarette consumption = 29). Smokers were younger than nonsmokers and more likely to be male and of lower socioeconomic status. Over a median follow-up of 21.4 years, 273 (18.4%) patients developed cancer. Baseline smoking was associated with a ∼40% excess adjusted risk of cancer; ∼25% after accounting for death as a competing event. Considering changes in smoking during follow-up, the excess risk was confined to persistent smokers (adjusted HR 1.75; 95% confidence interval [CI], 1.22-2.50), whereas post- (HR 1.14; 95% CI, 0.80-1.62) and pre-myocardial infarction quitters (HR 1.02; 95% CI, 0.71-1.47) were comparable with never smokers. Among persistent smokers, each reduction of 10 cigarettes relative to pre-myocardial infarction consumption was associated with a ∼10% reduced adjusted risk. Among young survivors of first myocardial infarction followed-up longitudinally, smoking cessation is associated with lower risk of cancer. Reducing consumption among smokers may also be beneficial. Copyright © 2017 Elsevier Inc. All rights reserved.

Adenoviral short hairpin RNA therapy targeting phosphodiesterase 5a relieves cardiac remodeling and dysfunction following myocardial infarction

Science.gov (United States)

Li, Longhu; Haider, Husnain Kh.; Wang, Linlin; Lu, Gang

2012-01-01

We previously showed that treatment with tadalafil, a long-acting phosphodiesterase-5a (PDE5a) inhibitor, effectively prevented adverse left ventricular (LV) remodeling of the infarcted heart. We hypothesized that short-hairpin RNA (shRNA) therapy targeting PDE5a would simulate the effects of pharmacological intervention for treatment of postinfarction LV remodeling and dysfunction. Experimental model of myocardial infarction was developed in female mice by permanent ligation of left coronary artery. Immediately after that, an adenoviral vector encoding for shRNA sequence targeting PDE5a (Ad-shPDE5a) was injected intramyocardially, which specifically inhibited PDE5a in the heart. Four weeks later, Ad-shPDE5a treated mice showed significant mitigation of the left ventricle (LV) dilatation and dysfunction as indicated by smaller LV cavity and more preserved ejection fraction and fractional shortening. Infarction size and fibrosis were significantly reduced in Ad-shPDE5a-treated mice. Additionally, more salvaged cardiomyocytes, significantly reduced collagen contents, and higher blood vessel density were observed in Ad-shPDE5a-treated mice. The cytoprotective effects of Ad-shPDE5a were demonstrated in vitro in Ad-shPDE5a transfected cardiomyocytes cultured under oxygen glucose deprivation. Among downstream mediators of PDE5a signaling, cyclic GMP (cGMP) and cGMP-dependent protein kinase G (PKG) were activated with concomitant reduction in caspase-3 activity. However, no significant change in PKA and cAMP activities were observed in Ad-shPDE5a-treated hearts. Inhibition with shRNA improved cardiac remodeling and dysfunction by reducing infarction size and cardiac fibrosis and increased cGMP and PKG activity. These findings suggest that PDE5 inhibition with Ad-shPDE5a is a novel approach for treatment of myocardial infarction. PMID:22447941

Salvianolic acid A alleviates ischemic brain injury through the inhibition of inflammation and apoptosis and the promotion of neurogenesis in mice.

Science.gov (United States)

Chien, Mei-Yin; Chuang, Cheng-Hung; Chern, Chang-Ming; Liou, Kou-Tong; Liu, Der-Zen; Hou, Yu-Chang; Shen, Yuh-Chiang

2016-10-01

Salvianolic acid A (SalA), a chemical type of caffeic acid trimer, has drawn great attention for its potent bioactivities against ischemia-induced injury both in vitro and in vivo. In this study, we evaluated SalA's protective effects against acute ischemic stroke by inducing middle cerebral artery occlusion/reperfusion (MCAO) injuries in mice. Treatment of the mice with SalA (50 and 100μg/kg, i.v.) at 2h after MCAO enhanced their survival rate, improved their moving activity, and ameliorated the severity of brain infarction and apoptosis seen in the mice by diminishing pathological changes such as the extensive breakdown of the blood-brain barrier (BBB), nitrosative stress, and the activation of an inflammatory transcriptional factor p65 nuclear factor-kappa B (NF-κB) and a pro-apoptotic kinase p25/Cdk5. SalA also intensively limited cortical infarction and promoted the expression of neurogenesis protein near the peri-infarct cortex and subgranular zone of the hippocampal dentate gyrus by compromising the activation of GSK3β and p25/Cdk5, which in turn upregulated β-catenin, doublecortin (DCX), and Bcl-2, most possibly through the activation of PI3K/Akt signaling via the upregulation of brain-derived neurotrophic factor. We conclude that SalA blocks inflammatory responses by impairing NF-κB signaling, thereby limiting inflammation/nitrosative stress and preserving the integrity of the BBB; SalA also concomitantly promotes neurogenesis-related protein expression by compromising GSK3β/Cdk5 activity to enhance the expression levels of β-catenin/DCX and Bcl-2 for neuroprotection. Copyright © 2016 Elsevier Inc. All rights reserved.

Perfusion scintigraphy in acute myocardial infarction

International Nuclear Information System (INIS)

Schricke, U.; Schwaiger, M.; Kastrati, A.; Schoemig, A.

1999-01-01

The Tc-99m sestamibi perfusion SPECT scintigraphy in acute myocardial infarction is a feasible method to assess the size of area at risk and the residual blood flow to this area as the most important determinants of final infarct size without any delay in treatment. In combination with a follow-up study final infarct size as well as myocardial salvage can be quantified. Clinical indications for the use of Tc-99m sestamibi scintigraphy are the noninvasive identification of arterial occlusion in patients suspected to acute myocardial infarction without electrocardiographic ST-elevation and the assessment of reperfusion success. In clinical trials Tc-99m sestamibi scintigraphy has proven to be a useful method to assess the impact of varying reperfusion therapies. The present review article discusses the indication, the study protocol, the interpretation of results and the clinical and scientifically importance of this method. (orig.) [de

Detection of infarct size safety threshold for left ventricular ejection fraction impairment in acute myocardial infarction successfully treated with primary percutaneous coronary intervention.

Science.gov (United States)

Sciagrà, Roberto; Cipollini, Fabrizio; Berti, Valentina; Migliorini, Angela; Antoniucci, David; Pupi, Alberto

2013-04-01

In acute myocardial infarction (AMI) treated by primary percutaneous coronary intervention (PCI), there is a direct relationship between myocardial damage and consequent left ventricular (LV) functional impairment. It is however unclear whether there is a safety threshold below which infarct size does not significantly affect LV ejection fraction (EF). The aim of this study was to evaluate the relationship between infarct size and LVEF in AMI patients treated by successful PCI using a specific statistical approach to identify a possible safety threshold. Among patients with recent AMI submitted to perfusion gated single photon emission computed tomography (SPECT) to define the infarct size, the data of 427 subjects with sizable infarct size were considered. The relationship between infarct size and LVEF was analysed using a simple segmented regression (SSR) model and an iterative algorithm based on robust least squares (RLS) for parameter estimation. The RLS algorithm detected two break points in the SSR model, set at infarct size values of 11.0 and 51.5 %. Because the slope coefficients of the two extreme segments of the regression line were not significant, by constraining such segments to zero slope in the SSR model, the lower break point was identified at infarct size = 8 % and the upper one at 45 %. Using a rigorous statistical approach, it is possible to demonstrate that below a threshold of 8 % the infarct size apparently does not affect the LVEF and therefore a safety threshold could be set at this value. Furthermore, the same analysis suggests that the relationship between infarct size and LVEF impairment is lost for an infarct size > 45 %.

Scintigraphic characteristics of experimental myocardial infarct extension

International Nuclear Information System (INIS)

Kronenberg, M.W.; Wooten, N.E.; Friesinger, G.C.; Page, D.L.; Higgins, S.B.; Collins, J.C.; O'Connor, J.L.; Price, R.R.; Brill, A.B.

1979-01-01

Technetium-99m-stannous pyrophosphate scintiphotos were evaluated for diagnosing and quantitating myocardial infarct (MI) extension in sedated dogs. Infarction and extension were produced by serial left anterior descending coronary artery ligations at 0 and 48 hours. We compared serial scintiphoto data with regional myocardial blood flow (MBF) (microsphere technique) and infarct histopathology. In eight control dogs, the scintigraphic MI area was stable at 24, 48, and 72 hours. In each of 11 dogs undergoing extension, the MI area increased after the 48-hour occlusion, averaging a 48.9% increase (p < 0.001). Grossly, most extensions were mixtures of confluent necrosis and moderate (patchy) necrosis. MBF to confluent infarct tissue decreased significantly, allowing the documentation of extension by totaling the grams of newly flow-deprived tissue, but patchy infarct tissue had little flow deprivation, making it difficult to quantitate this type of extension accurately by flow criteria alone. Rarely, extension could be diagnosed using conventional histologic criteria. We concluded that the scintiphoto MI area was related quantitatively to infarct weight in both control and extension. However, it was not possible to determine that an increase in the MI scintiphoto area was an accurate predictor of the degree of extension using independent flow or pathologic criteria

Effects of total saponins from Trillium tschonoskii rhizome on grey and white matter injury evaluated by quantitative multiparametric MRI in a rat model of ischemic stroke.

Science.gov (United States)

Li, Manzhong; Ouyang, Junyao; Zhang, Yi; Cheng, Brian Chi Yan; Zhan, Yu; Yang, Le; Zou, Haiyan; Zhao, Hui

2018-04-06

Trillium tschonoskii rhizome (TTR), a medicinal herb, has been traditionally used to treat traumatic brain injury and headache in China. Although the potential neuroprotective efficacy of TTR has gained increasing interest, the pharmacological mechanism remains unclear. Steroid saponins are the main bioactive components of the herb. To investigate the protective and repair-promoting effects of the total saponins from TTR (TSTT) on grey and white matter damages in a rat model of middle cerebral artery occlusion (MCAO) using magnetic resonance imaging (MRI) assay. Ischemic stroke was induced by MCAO. TSTT and Ginaton (positive control) were administered orally to rats 6h after stroke and daily thereafter. After 15 days of treatment, the survival rate of each group was calculated. We then conducted neurological deficit scores and beam walking test to access the neurological function after ischemic stroke. Subsequently, T2-weighted imaging (T2WI) and T2 relaxometry mapping were performed to measure infarct volume and grey and white matter integrity, respectively. Moreover, diffusion tensor imaging (DTI) was carried out to evaluate the grey and white matter microstructural damage. Additionally, arterial spin labelling (ASL) - cerebral blood flow (CBF) and magnetic resonance angiography (MRA) images provided dynamic information about vascular hemodynamic dysfunction after ischemic stroke. Finally, haematoxylin and eosin (HE) staining was carried out to evaluate the stroke-induced pathological changes in the brain. The survival rate and neurological behavioural outcomes (Bederson scores and beam walking tests) were markedly ameliorated by TSTT (65mg/kg) treatment within 15 days after ischemic stroke. Moreover, T2WI and T2 relaxometry mapping showed that TSTT (65mg/kg) significantly reduced infarct volume and attenuated grey and white matter injury, respectively, which was confirmed by histopathological evaluation of brain tissue. The results obtained from DTI showed that

Estimation of infarct size by myocardial emission computed tomography with thallium-201 and its relation to creatine kinase-MB release after myocardial infarction in man

International Nuclear Information System (INIS)

Tamaki, S.; Nakajima, H.; Murakami, T.

1982-01-01

Emission computed tomography (ECT) for thallium-201 ( 201 Tl) myocardial imaging was evaluated in estimating infarct size (IS). In 18 patients in whom IS was estimated enzymatically at the time of the acute episode, planar 201 Tl perfusion scintigraphy and ECT with a rotating gamma camera were performed 4 weeks after the first myocardial infarction. From the size of 201 Tl perfusion defects, the infarct area in planar images and the infarct volume in reconsturcted ECT images were measured by computerized planimetry. When scintigraphic IS was compared with the accumulated creatine kinase-MB isoenzyme release (CK-MBr), infarct volume determined from ECT correlated closely with CK-MBr (r=0.89), whereas infarct area measured from planar images correlated less satisfactorily with the enzymatic IS (for an average infarct area from three views, r=0.69; for the largest infarct area, r=0.73). Although conventional scintigraphic evaluation is useful for detecting and localizing infarction, quantification of ischemic injury with this two-dimensional technique has a significant inherent limitation. The ECT approach can provide a more accurate three-dimensional quantitative estimate of infarction, and can corroborate the enzymatic estimate of IS

Estimation of infarct size by myocardial emission computed tomography with 201Tl and its relation to creatine kinase-MB release after myocardial infarction in man

International Nuclear Information System (INIS)

Tamaki, S.; Nakajima, H.; Murakami, T.

1982-01-01

We evaluated emission computed tomography (ECT) 201 Tl myocardial imaging in estimating infarct size (IS). In 18 patients in whom IS was estimated enzymatically at the time of the acute episode, planar 201 Tl perfusion scintigraphy and ECT with a rotating gamma camera were performed 4 weeks after the first myocardial infarction. From the size of 201 Tl perfusion defects, the infarct area in planar images and the infarct volume in reconstructed ECT images were measured by computerized planimetry. When scintigraphic IS was compared with the accumulated creatine kinase-MB isoenzyme release (CK-MBr), infarct volume determined from ECT correlated closely with CK-MBr (r . 0.89), whereas infarct area measured from planar images correlated less satisfactorily with the enzymatic IS (for an average infarct area from three views, r . 0.69; for the largest infarct area, r . 0.73). Although conventional scintigraphic evaluation is useful for detecting and localizing infarction, quantification of ischemic injury with this two-dimensional technique has a significant inherent limitation. The ECT approach can provide a more accurate three-dimensional quantitative estimate of infarction, and can corroborate the enzymatic estimate of IS

Evaluation of cat brain infarction model using microPET

Energy Technology Data Exchange (ETDEWEB)

Lee, Jong Jin; Lee, Dong Soo; Kim, Yun Hui; Hwang, Do Won; Kim, Jin Su; Chung, June Key; Lee, Myung Chul [College of Medicine, Seoul National Univ., Seoul (Korea, Republic of); Lim, Sang Moo [Korea Institite of Radiological and Medical Sciences, Seoul (Korea, Republic of)

2004-12-01

PET has some disadvantage in the imaging of small animal due to poor resolution. With the advent of microPET scanner, it is possible to image small animals. However, the image quality was not good enough as human image. Due to larger brain, cat brain imaging was superior to mouse or rat. In this study, we established the cat brain infarction model and evaluate it and its temporal change using microPET scanner. Two adult male cats were used. Anesthesia was done with xylazine and ketamine HCI. A burr hole was made at 1 cm right lateral to the bregma. Collagenase type IV 10 {mu}l was injected using 30 G needle for 5 minutes to establish the infarction model. {sup 18}F-FDG microPET (Concorde Microsystems Inc., Knoxville, TN) scans were performed 1, 11 and 32 days after the infarction. In addition, {sup 18}F-FDG PET scans were performed using human PET scanner (Gemini, Philips medical systems, CA, USA) 13 and 47 days after the infarction. Two cat brain infarction models were established. The glucose metabolism of an infarction lesion improved with time. An infarction lesion was also distinguishable in the human PET scan. We successfully established the cat brain infarction model and evaluated the infarcted lesion and its temporal change using {sup 18}F-FDG microPET scanner.

Evaluation of cat brain infarction model using microPET

International Nuclear Information System (INIS)

Lee, Jong Jin; Lee, Dong Soo; Kim, Yun Hui; Hwang, Do Won; Kim, Jin Su; Chung, June Key; Lee, Myung Chul; Lim, Sang Moo

2004-01-01

PET has some disadvantage in the imaging of small animal due to poor resolution. With the advent of microPET scanner, it is possible to image small animals. However, the image quality was not good enough as human image. Due to larger brain, cat brain imaging was superior to mouse or rat. In this study, we established the cat brain infarction model and evaluate it and its temporal change using microPET scanner. Two adult male cats were used. Anesthesia was done with xylazine and ketamine HCI. A burr hole was made at 1 cm right lateral to the bregma. Collagenase type IV 10 μl was injected using 30 G needle for 5 minutes to establish the infarction model. 18 F-FDG microPET (Concorde Microsystems Inc., Knoxville, TN) scans were performed 1, 11 and 32 days after the infarction. In addition, 18 F-FDG PET scans were performed using human PET scanner (Gemini, Philips medical systems, CA, USA) 13 and 47 days after the infarction. Two cat brain infarction models were established. The glucose metabolism of an infarction lesion improved with time. An infarction lesion was also distinguishable in the human PET scan. We successfully established the cat brain infarction model and evaluated the infarcted lesion and its temporal change using 18 F-FDG microPET scanner

Intense correlation between brain infarction and protein-conjugated acrolein.

Science.gov (United States)

Saiki, Ryotaro; Nishimura, Kazuhiro; Ishii, Itsuko; Omura, Tomohiro; Okuyama, Shigeru; Kashiwagi, Keiko; Igarashi, Kazuei

2009-10-01

We recently found that increases in plasma levels of protein-conjugated acrolein and polyamine oxidases, enzymes that produce acrolein, are good markers for stroke. The aim of this study was to determine whether the level of protein-conjugated acrolein is increased and levels of spermine and spermidine, the substrates of acrolein production, are decreased at the locus of infarction. A unilateral infarction was induced in mouse brain by photoinduction after injection of Rose Bengal. The volume of the infarction was analyzed using the public domain National Institutes of Health image program. The level of protein-conjugated acrolein at the locus of infarction and in plasma was measured by Western blotting and enzyme-linked immunosorbent assay, respectively. The levels of polyamines at the locus of infarction and in plasma were measured by high-performance liquid chromatography. The level of protein-conjugated acrolein was greatly increased, and levels of spermine and spermidine were decreased at the locus of infarction at 24 hours after the induction of stroke. The size of infarction was significantly decreased by N-acetylcysteine, a scavenger of acrolein. It was also found that the increases in the protein-conjugated acrolein, polyamines, and polyamine oxidases in plasma were observed after the induction of stroke. The results indicate that the induction of infarction is well correlated with the increase in protein-conjugated acrolein at the locus of infarction and in plasma.

[A case of infectious mononucleosis with splenic infarction].

Science.gov (United States)

Kobe, Daisuke; Nakatani, Toshiya; Fujinaga, Yukihisa; Seki, Kenichiro; Saikawa, Soichiro; Sawada, Yasuhiko; Sato, Yoshiki; Nagamatsu, Shinsaku; Matsuo, Hideki; Kikuchi, Eiryo

2013-08-01

A 22-year-old man complaining of persisting high fever and right hypochondralgia was admitted to our hospital for infectious mononucleosis with splenic infarction detected by computed tomography. The splenic infarction deteriorated with a marked elevation of inflammatory parameters. This necessitated the commencement of methylprednisolone pulse therapy, resulting in prompt amelioration of inflammation and a reduction in cytokine levels. Including our case, only 9 cases of mononucleosis with splenic infarction have been reported to date; however, splenic infarction should be considered because it is a significant complication of infectious mononucleosis.

Angiotensin II Type 2 Receptor Agonist Experts Sustained Neuroprotective Effects In Aged Rats

DEFF Research Database (Denmark)

Sumners, Colin; Isenberg, Jacob; Harmel, Allison

2016-01-01

OBJECTIVE: The renin angiotensin system is a promising target for stroke neuroprotection and therapy through activation of angiotensin type II receptors (AT2R). The selective non-peptide AT2R agonist, Compound 21 (C21), has been shown to exhibit neuroprotection and improve stroke outcomes...... in preclinical studies, effects that likely involve neurotropic actions. However, these beneficial actions of C21 have not been demonstrated to occur beyond 1 week post stroke. The objective of this study was to determine if systemic administration of C21 would exert sustained neuroprotective effects in aged...... min), 24 h, and 48 h after stroke. Infarct size was assessed by magnetic resonance imaging at 21 days post MCAO. Animals received blinded neurological exams at 4 h, 24 h, 72 h, 7d, 14d, and 21d post-MCAO. RESULTS: Systemic treatment with C21 after stroke significantly improved neurological function...

Infarct size in patients with acute myocardial infarction estimated by emission computed tomography with technetium-99m pyrophosphate. Relation to creatine phosphokinase release

Energy Technology Data Exchange (ETDEWEB)

Maruyama, Jun-ichi; Onodera, Sokichi; Imura, Suguru; Marutani, Yoshiaki; Takahori, Takashi; Nasuhara, Koh-ichi

1986-09-01

To evaluate the usefulness of single photon emission computed tomography (SPECT) with technetium-99m-pyrophosphate (/sup 99m/Tc-PYP) for estimating infarct size, we compared SPECT data with maximum creatine phosphokinase values. Background threshold was established in a series of phantom experiments. When a 40 % cut-off was applied, the SPECT data most closely approximated actual phantom volumes. Therefore, the 40 % cut-off level was used in the present study. In 10 patients with acute myocardial infarction, planar /sup 99m/Tc-PYP myocardial scintigraphy and SPECT using a rotating gamma camera were performed two days after the initial myocardial infarction episode. The maximum creatine phosphokinase value (CPKmax) was also measured repeatedly following the episode. When the infarct size measured by SPECT using transaxial images and calculated by the pixel counts, it correlated very closely with CPKmax (r = 0.94). Most studies so far have reported that the CPKmax level reflects infarct size. We conclude that the infarct size as measured by /sup 99m/Tc-PYP SPECT closely approximates the actual infarct size, and that this method is useful to determine the severity of infarcts clinically. Among the 10 patients in this series, three of five with infarcts greater than 60 ml died of pump failure. Therefore, we may be able to predict prognosis after accumulating more such cases and improving the methodology.

Changes in somatotropic hormone secretion in patients with acute myocardial infarct

International Nuclear Information System (INIS)

Milanov, S.; Milkov, V.; Atanasov, I.; Sotirov, I.; Kamenova, Ts.

1982-01-01

Secretion of somatotropic hormone (STH) was estimated by radioimmunoassay during intravenous glucose-tolerance test (IGTT) in 17 patients with acute myocardial infarct (AMI) and 10 patients with chronic ischemic heart disease, without evidence of recent myocardial infarct. In both groups of patients the basal STH levels were elevated, as compared to those in normal individuals, with statistical significance (p<0.001). During the IGTT, somatotropic hormone in AMI patients was slightly reduced, which was out of proportion to the blood glucose changes. During IGTT in patients with chronic ischemic heart disease, the somatotropic hormone secretion, though increased, followed the blood glucose changes. These changes in STH secretion during IGTT in AMI patients are indicative of impaired hypothalamo-pituitary interrelations mediated by central nervous route. (author)

[Analysis of 58 neonatal cases with cerebral infarction].

Science.gov (United States)

Li, Zhi-hua; Chen, Chao

2013-01-01

Cerebral infarction (CI) is one of severe diseases of central nervous system in neonates, and some infants with CI could have poor prognosis in the long term. This study aimed to analyze the clinical data and prognosis of all neonatal cases with cerebral infarction in recent years and to help future clinical work. Totally 58 neonatal cases with CI admitted to NICU of the hospital from January 1999 to December 2010 were included in this study. We analyzed all clinical data and prognosis by retrospective analysis. Fifty-two term babies and six preterm babies were included. There were altogether 51 cases with asphyxia and 7 with hemorrhagic cerebral infarction. Perinatal hypoxia-ischemia was the most common high-risk factor and it accounted for 46.6%. Seizure was the most frequent initial symptom and the most common clinical manifestation (accounted for 77.6%), and it was followed by intermittent cyanosis, apnea and lethargy. Cerebral CT scan and magnetic resonance imaging were major methods to help to make the diagnosis and they also had close relation with prognosis. Diffusion weighted imaging was very helpful to diagnose infarction in early stage. Left middle cerebral artery was the most common artery to be involved. Supportive therapy and symptomatic treatment were the main methods in the acute stage of neonatal cerebral infarction. Those babies with poor prognosis mostly had large infarction involving cerebral hemisphere, thalamus and basal ganglia. Neonatal cerebral infarction was a severe brain injury affecting long tern nervous system prognosis. Perinatal hypoxia was the most common high-risk factor and seizure was the most frequent initial symptom. Diffusion weighted imaging was valuable to diagnose infarction in early stage. Most of infants with poor prognosis had large infarction involving hemisphere, thalamus and basal ganglia. Early diagnosis with brain imaging would be helpful for rehabilitation therapy and improving prognosis.

TNF-Like Weak Inducer of Apoptosis Aggravates Left Ventricular Dysfunction after Myocardial Infarction in Mice

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Kai-Uwe Jarr

2014-01-01

Full Text Available Background. TNF-like weak inducer of apoptosis (TWEAK has recently been shown to be potentially involved in adverse cardiac remodeling. However, neither the exact role of TWEAK itself nor of its receptor Fn14 in this setting is known. Aim of the Study. To analyze the effects of sTWEAK on myocardial function and gene expression in response to experimental myocardial infarction in mice. Results. TWEAK directly suppressed the expression of PGC-1α and genes of oxidative phosphorylation (OXPHOS in cardiomyocytes. Systemic sTWEAK application after MI resulted in reduced left ventricular function and increased mortality without changes in interstitial fibrosis or infarct size. Molecular analysis revealed decreased phosphorylation of PI3K/Akt and ERK1/2 pathways associated with reduced expression of PGC-1α and PPARα. Likewise, expression of OXPHOS genes such as atp5O, cycs, cox5b, and ndufb5 was also reduced. Fn14 -/- mice showed significantly improved left ventricular function and PGC-1α levels after MI compared to their respective WT littermates (Fn14 +/+. Finally, inhibition of intrinsic TWEAK with anti-TWEAK antibodies resulted in improved left ventricular function and survival. Conclusions. TWEAK exerted maladaptive effects in mice after myocardial infarction most likely via direct effects on cardiomyocytes. Analysis of the potential mechanisms revealed that TWEAK reduced metabolic adaptations to increased cardiac workload by inhibition of PGC-1α.

[Reduction of in-hospital mortality and improved secondary prevention after acute myocardial infarction. First results from the registry of secondary prevention after acute myocardial infarction (SAMI)].

Science.gov (United States)

Tebbe, U; Messer, C; Stammwitz, E; The, G S; Dietl, J; Bischoff, K-O; Schulten-Baumer, U; Tebbenjohanns, J; Gohlke, H; Bramlage, P

2007-07-30

In hospital mortality of acute myocardial infarction (AMI) has been reduced due to the availability of better therapeutic strategies. But there is still a gap between mortality rates in randomised trials and daily clinical practice. Thus, it was aim of the present registry to document the course and outcome of patients with AMI and to improve patient care by implementing recent guidelines. In a nationwide registry study in hospitals in Germany with a cardiology unit or an internal medicine department data on consecutive patients were recorded for six to twelve months at admission, discharge and during a follow-up of one year. From 02/2003 until 10/2004 a total of 5,353 patients with acute myocardial infarction (65.7 % male, mean age of 67.6 +/- 17.7 years; 55.1 % of them with ST elevation myocardial infarction (STEMI) were included in the registry. Of the patients with STEMI, 76.6 % underwent acute intervention, 37.1 % had thrombolysis, 69.7 % percutaneous transluminal coronary angioplasty (PTCA). 40.0 % of those with non-Stemi (NSTEMI) had an acute intervention, 6.6 % thrombolysis, 73.5 % PTCA. Recommended secondary prevention consisted of ASS (93.2 %), beta-blockers (93.0 %), CSE-inhibitors (83.5 %), ACE-inhibitors (80.9 %) and clopidogrel (74.0 %). In-hospital mortality was 10.5 % (STEMI) and 7.4 % (NSTEMI). The 9 % mortality among patients with acute myocardial infarction treated in the hospitals participating in the SAMI registry is low compared to that in similar collectives. The high number of patients who had thrombofibrinolysis and coronary interventions as well as the early initiation of drug therapy contributed to these results. Medical treatment in the prehospital phase of these patients remains still insufficient and to a substantial extent contributes to the mortality of acute myocardial infarction.

Reducing Microvascular Dysfunction in Revascularized Patients with ST-Elevation Myocardial Infarction by Off-Target Properties of Ticagrelor versus Prasugrel. Rationale and Design of the REDUCE-MVI Study

NARCIS (Netherlands)

G.N. Janssens (Gladys N.); M.A.H. van Leeuwen (Maarten); N.W. van der Hoeven (Nina W.); G.A. de Waard (Guus); R. Nijveldt (Robin); R. Diletti (Roberto); F. Zijlstra (Felix); C. Von Birgelen (Clemens); J. Escaned (Javier); M. Valgimigli (Marco); N. van Royen (Niels)

2016-01-01

textabstractMicrovascular injury is present in a large proportion of patients with ST-elevation myocardial infarction (STEMI) despite successful revascularization. Ticagrelor potentially mitigates this process by exerting additional adenosine-mediated effects. This study aims to determine whether

DESTINY-S: attitudes of physicians toward disability and treatment in malignant MCA infarction.

Science.gov (United States)

Neugebauer, Hermann; Creutzfeldt, Claire J; Hemphill, J Claude; Heuschmann, Peter U; Jüttler, Eric

2014-08-01

Decompressive hemicraniectomy (DHC) reduces mortality and improves outcome after malignant middle cerebral artery (MCA) infarction but leaves a high number of survivors severely disabled. Attitudes among physicians toward the degree of disability that is considered acceptable and the impact of aphasia may play a major role in treatment decisions. DESTINY-S is a multicenter, international, cross-sectional survey among 1,860 physicians potentially involved in the treatment of malignant MCA infarction. Questions concerned the grade of disability, the hemisphere of the stroke, and the preferred treatment for malignant MCA infarction. mRS scores of 3 or better were considered acceptable by the majority of respondents (79.3%). Only few considered a mRS score of 5 still acceptable (5.8%). A mRS score of 4 was considered acceptable by 38.0%. Involved hemisphere (dominant vs. non-dominant) was considered a major clinical symptom influencing treatment decisions in 47.7% of respondents, also reflected by significantly different rates for DHC as preferred treatment in dominant versus non-dominant hemispheric infarction (46.9 vs. 72.9%). Significant differences in acceptable disability and treatment decisions were found among geographic regions, medical specialties, and respondents with different work experiences. Little consensus exists among physicians regarding acceptable outcome and therapeutic management after malignant MCA infarction, and physician's recommendations do not correlate with available evidence. We advocate for a decision-making process that balances scientific evidence, patient preference, and clinical expertise.

Skull infarction in a patient with malignant fibrous histiocytoma.

Science.gov (United States)

Nagle, C E; Morayati, S J; LeDuc, M A

1987-09-01

The authors describe a case of a skull infarction initially suspected to be an isolated, remote metastasis in a patient diagnosed with soft tissue malignant fibrous histiocytoma. Osseous malignant fibrous histiocytoma has been reported to occur within a bone infarction but the presence of a benign bone infarction remote from a soft tissue malignant fibrous histiocytoma has not been reported previously. Bone infarctions and malignant fibrous histiocytomas are briefly reviewed.

Culprit versus multivessel coronary intervention in ST-segment elevation myocardial infarction: a meta-analysis of randomized trials.

Science.gov (United States)

Vaidya, Satyanarayana R; Qamar, Arman; Arora, Sameer; Devarapally, Santhosh R; Kondur, Ashok; Kaul, Prashant

2018-03-01

The 2015 American College of Cardiology/American Heart Association update on primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) recommended PCI of the non-infarct-related artery at the time of primary PCI (class IIb recommendation). Despite evidence supporting complete revascularization in STEMI, its benefit on mortality rates is uncertain. We searched all available databases for randomized controlled trials comparing complete multivessel percutaneous coronary intervention (CMV PCI) with infarct-artery-only revascularization in patients with STEMI. Summary risk ratios and 95% confidence intervals (CIs) were calculated for both the efficacy and safety outcomes. Nine randomized controlled trials fulfilled the inclusion criteria, yielding 2991 patients. Follow-up periods ranged from 6 to 36 months. Compared with infarct-related artery-only PCI, CMV PCI was associated with significantly lower rates of major adverse cardiac events [relative risk (RR)=0.54, 95% CI=0.41-0.71; P<0.00001], cardiovascular mortality (RR=0.48, 95% CI=0.28-0.80; P=0.005), and repeat revascularization (RR=0.38, 95% CI=0.30-0.47; P<0.00001). Although, contrast-induced nephropathy and major bleed rates were comparable between both groups, CMV PCI failed to show any reduction in all-cause mortality (RR=0.75, 95% CI=0.53-1.07; P=0.11) and nonfatal myocardial infarction (RR=0.69, 95% CI=0.43-1.10; P=0.12). Our results suggest that in patients with STEMI and multivessel disease, complete revascularization is safe, and is associated with reduced risks of major adverse cardiac events and cardiac death along with a reduced need for repeat revascularization. However, it showed no beneficial effect on all-cause mortality and nonfatal myocardial infarction.

Three-dimension structure of ventricular myocardial fibers after myocardial infarction

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Li Libin

2010-11-01

Full Text Available Abstract Background To explore the pathological changes of three-dimension structure of ventricular myocardial fibers after anterior myocardial infarction in dog heart. Methods Fourteen acute anterior myocardial infarction models were made from healthy dogs (mean weight 17.6 ± 2.5 kg. Six out of 14 dogs with old myocardial infarction were sacrificed, and their hearts were harvested after they survived the acute anterior myocardial infarction for 3 months. Each heart was dissected into ventricular myocardial band (VMB, morphological characters in infarction region were observed, and infarct size percents in descending segment and ascending segment were calculated. Results Six dog hearts were successfully dissected into VMB. Uncorresponding damages in myocardial fibers of descending segment and ascending segment were found in apical circle in anterior wall infarction. Infarct size percent in the ascending segment was significantly larger than that in the descending segment (23.36 ± 3.15 (SD vs 30.69 ± 2.40%, P = 0.0033; the long axis of infarction area was perpendicular to the orientation of myocardial fibers in ascending segment; however, the long axis of the infarction area was parallel with the orientation of myocardial fibers in descending segment. Conclusions We found that damages were different in both morphology and size in ascending segment and descending segment in heart with myocardial infarction. This may provide an important insight for us to understand the mechanism of heart failure following coronary artery diseases.

Acute myocardial infarcts

International Nuclear Information System (INIS)

Just, H.

1988-01-01

Acute myocardial infarction is a major complication of stenosing coronary artery disease and constitutes the most frequent single cause of death. It is caused by thrombotic occlusion of one of the major epicardial coronary arterial branches in most cases. Sudden death due to ventricular fibrillation is responsible for the majority of early fatalities. In 60% of all fatal infarcts, death occurs within 1 h of the onset of pain. The final extension of myocardial necrosis is reached within 2-4 h. An integrated programme has therefore been developed for the supervision and treatment of patients suffering acute coronary attack; it has been shown that it can markedly lower infarct mortality. It includes mobile prehospital care, intensive care treatment in the hospital, and rehabilitative procedures for application during reconvalescence. Early antiarrhythmic treatment and myocardial reperfusion via fibrinolysis are the main therapeutic procedures in the earliest stage. In hospital an operating room and an operating team must be available round the clock for the performance of coronary angiography followed by percutaneous transluminal coronary angioplasty or bypass surgery, which can be safely carried out in the acute stage provided the indications are strictly observed. Mortality and morbidity can be significantly lowered and both life expectancy and quality of life can be remarkably improved. (orig.) [de

Low-Density Lipoprotein Receptor–Related Protein-1 Is a Therapeutic Target in Acute Myocardial Infarction

Directory of Open Access Journals (Sweden)

Stefano Toldo, PhD

2017-10-01

Full Text Available Low-density lipoprotein receptor–related protein-1 (LRP1 is a ubiquitous membrane receptor functioning as a scavenger and regulatory receptor, inducing anti-inflammatory and prosurvival signals. Based on the known structure–activity of the LRP1 receptor binding site, the authors synthesized a small peptide (SP16. SP16 induced a >50% reduction in infarct size (p < 0.001 and preservation of left ventricular systolic function (p < 0.001, and treatment with an LRP1 blocking antibody eliminated the protective effects of SP16. In conclusion, LRP1 activation with SP16 given within 30 min of reperfusion during experimental acute myocardial infarction leads to a cardioprotective signal reducing infarct size and preservation of cardiac systolic function.

Coronary collateral vessels in patients with previous myocardial infarction

International Nuclear Information System (INIS)

Nakatsuka, M.; Matsuda, Y.; Ozaki, M.

1987-01-01

To assess the degree of collateral vessels after myocardial infarction, coronary angiograms, left ventriculograms, and exercise thallium-201 myocardial scintigrams of 36 patients with previous myocardial infarction were reviewed. All 36 patients had total occlusion of infarct-related coronary artery and no more than 70% stenosis in other coronary arteries. In 19 of 36 patients with transient reduction of thallium-201 uptake in the infarcted area during exercise (Group A), good collaterals were observed in 10 patients, intermediate collaterals in 7 patients, and poor collaterals in 2 patients. In 17 of 36 patients without transient reduction of thallium-201 uptake in the infarcted area during exercise (Group B), good collaterals were seen in 2 patients, intermediate collaterals in 7 patients, and poor collaterals in 8 patients (p less than 0.025). Left ventricular contractions in the infarcted area were normal or hypokinetic in 10 patients and akinetic or dyskinetic in 9 patients in Group A. In Group B, 1 patient had hypokinetic contraction and 16 patients had akinetic or dyskinetic contraction (p less than 0.005). Thus, patients with transient reduction of thallium-201 uptake in the infarcted area during exercise had well developed collaterals and preserved left ventricular contraction, compared to those in patients without transient reduction of thallium-201 uptake in the infarcted area during exercise. These results suggest that the presence of viable myocardium in the infarcted area might be related to the degree of collateral vessels

Unilateral Thalamic Infarct Presenting as a Convulsive Seizure.

Science.gov (United States)

Kumar, Rajesh; Brohi, Hazim; Mughul, Afshan

2017-09-01

Lesions of the thalamus and those extending into midbrain can cause various types of movement disorders such as dystonia, asterixis and ballism-chorea. Seizures are rare manifestation of thalamic disorder. Occurrence of seizures in bilateral thalamic infarct has been reported; but seizures in unilateral thalamic infarct have been reported very rarely. Literature review showed only single case of perinatal unilateral thalamic infarct presenting with seizures. We are reporting a unique case of convulsive seizure at the onset of unilateral thalamic infarct in an adult male, which has never been reported to the best of our knowledge.

Splenic Infarction: An Under-recognized Complication of Infectious Mononucleosis?

Science.gov (United States)

Li, Yan; George, Ann; Arnaout, Sami; Wang, Jennifer P; Abraham, George M

2018-03-01

Splenic infarction is a rare complication of infectious mononucleosis. We describe 3 cases of splenic infarction attributed to infectious mononucleosis that we encountered within a 2-month period. We underscore the awareness of this potential complication of infectious mononucleosis and discuss the differential diagnosis of splenic infarction, including infectious etiologies. While symptomatic management is usually sufficient for infectious mononucleosis-associated splenic infarction, close monitoring for other complications, including splenic rupture, is mandated.

Multiple Thromboembolic Cerebral Infarctions from the Aorta in a Patient with Churg-Strauss Syndrome.

Science.gov (United States)

Okada, Hideo

2017-02-01

Ischemic stroke is a rare complication of Churg-Strauss syndrome (CSS) and its pathogenesis has not been well clarified yet. We report a case of cerebral infarction in a patient with CSS due to embolism from a thrombus on the wall of the aorta. A 39-year-old man had multiple cerebral infarctions with symptoms of mild left hemiparesis and reduced vision. He was clinically diagnosed to have CSS based on remarkable eosinophilia, history of asthma, sinusitis, pulmonary infiltrates, and histologically proven extravascular eosinophilic infiltrates in the specimen of gastric mucosa. Cerebral angiography did not show any stenotic lesions in cerebral arteries. A thrombus was detected on the wall of the aorta by transesophageal echocardiography, which was considered as the source of embolism. The thrombus resolved on follow-up examination 3 months after the onset of the stroke. This is the first case report on cerebral infarction caused by aortogenic thromboembolism in a CSS patient. Other than cerebral vasculitis, embolism from cardiovascular system, including the wall of the aorta, is a possible cause of cerebral infarctions in a CSS patient. Copyright © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Prognostic value of 123-IODO-heptadecanoic acid imaging in patients with acute myocardial infarction

International Nuclear Information System (INIS)

Stoddart, P.G.P.; Wilde, P.; Papouchado, M.

1987-01-01

This trial aimed to test if the half life of radioiodinated heptadecanoic acid (HDA) in acutely infarcted myocardium is of prognostic value. Twenty patients had an HDA scan and a MUGA scan within 6 days of acute myocardial infarction, eighteen of these had a visible defect on the HDA images. The mean half life of the areas of acute infarction (15.50 min +/-7.82 min) was significantly shorter than that of normal myocardium (20.77 min +/-4.00 min). The MUGA scan was repeated after 6 months in 15 patients. The mean acute infarct half life was longer in patients with an LVEF improvement of at least 5% at 6 months (16.92 min +/-10.56 min), compared to those with a deterioration of more than 5% (11.75 min +/-4.03 min), although the difference is not statistically significant. While the results in a few individuals suggested that the half life may be of prognostic significance, the variable response of the group reduced the ability of the half life to act as a prognostic indicator. Improvements in imaging and background subtraction techniques may be necessary before the half life is of practical value. (orig.)

Overexpression of Cx43 in cells of the myocardial scar: Correction of post-infarct arrhythmias through heterotypic cell-cell coupling.

Science.gov (United States)

Roell, Wilhelm; Klein, Alexandra M; Breitbach, Martin; Becker, Torsten S; Parikh, Ashish; Lee, Jane; Zimmermann, Katrin; Reining, Shaun; Gabris, Beth; Ottersbach, Annika; Doran, Robert; Engelbrecht, Britta; Schiffer, Miriam; Kimura, Kenichi; Freitag, Patricia; Carls, Esther; Geisen, Caroline; Duerr, Georg D; Sasse, Philipp; Welz, Armin; Pfeifer, Alexander; Salama, Guy; Kotlikoff, Michael; Fleischmann, Bernd K

2018-05-08

Ventricular tachycardia (VT) is the most common and potentially lethal complication following myocardial infarction (MI). Biological correction of the conduction inhomogeneity that underlies re-entry could be a major advance in infarction therapy. As minimal increases in conduction of infarcted tissue markedly influence VT susceptibility, we reasoned that enhanced propagation of the electrical signal between non-excitable cells within a resolving infarct might comprise a simple means to decrease post-infarction arrhythmia risk. We therefore tested lentivirus-mediated delivery of the gap-junction protein Connexin 43 (Cx43) into acute myocardial lesions. Cx43 was expressed in (myo)fibroblasts and CD45 + cells within the scar and provided prominent and long lasting arrhythmia protection in vivo. Optical mapping of Cx43 injected hearts revealed enhanced conduction velocity within the scar, indicating Cx43-mediated electrical coupling between myocytes and (myo)fibroblasts. Thus, Cx43 gene therapy, by direct in vivo transduction of non-cardiomyocytes, comprises a simple and clinically applicable biological therapy that markedly reduces post-infarction VT.

Cardioprotective effect of amlodipine in oxidative stress induced by experimental myocardial infarction in rats

Directory of Open Access Journals (Sweden)

Sudhira Begum

2007-12-01

Full Text Available The present study investigated whether the administration of amlodipine ameliorates oxidative stress induced by experimental myocardial infarction in rats. Adrenaline was administered and myocardial damage was evaluated biochemically [significantly increased serum aspertate aminotransferase (AST, lactate dehydrogenase (LDH and malondialdehyde (MDA levels of myocardial tissue] and histologically (morphological changes of myocardium. Amlodipine was administered as pretreatment for 14 days in adrenaline treated rats. Statistically significant amelioration in all the biochemical parameters supported by significantly improved myocardial morphology was observed in amlodipine pretreatment. It was concluded that amlodipine afforded cardioprotection by reducing oxidative stress induced in experimental myocardial infarction of catecholamine assault.

NMR imaging of cerebral infarction

International Nuclear Information System (INIS)

Takusagawa, Yoshihiko; Yamaoka, Naoki; Doi, Kazuaki; Okada, Keisei

1987-01-01

One hundred and five patients with cerebral infarction were studied by nuclear magnetic resonance (NMR) CT (resistive type of magnet with strength of 0.1 tesla) and X-ray CT. Pulse sequences used saturation recovery (Tr = 600 mSec), Inversion recovery (Tr = 500 mSec, Td = 300 mSec) and spin echo (Tr = 1500 mSec, Te = 40, 80, 120, 160 mSec). Fifteen cases were examined by NMR-CT within 24 hours from onset. Proton NMR imaging could not detect cerebral ischemia as early as 2 hours after onset, but except could detect the lesions in Se image the area of cerebral infarct 3 hours after onset. After 5 hours from onset image changes in SE were evident and corresponded to the area of cerebral infarct, but image changes in IR could not fully delineate the infarcted area. NMR images of 41 year-old woman with cerebral embolism by MCA trunck occlusion associated with mitral stenosis were presented, and NMR-CT was examined 10 hours, 9th and 43th days after episode of MCA occlusion. Sixty patents (64 times) with lacunar infarction were studied by NMR-CT and X-ray CT. The inversion recovery images were used mainly for detection of lesions and comparison with X-ray CT. In 160 lesions which were detected by NMR-CT or X-ray CT, could 156 lesions be detected by NMR-CT and 78 lesions by X-ray CT. Inversion recovery images were more useful for detection of lacunes than X-ray CT. Calculated T1 and T2 values prolonged with time course from onset. (author)

Acute myocardial infarct imaging with indium-111-labeled monoclonal antimyosin Fab

International Nuclear Information System (INIS)

Khaw, B.A.; Yasuda, T.; Gold, H.K.; Leinbach, R.C.; Johns, J.A.; Kanke, M.; Barlai-Kovach, M.; Strauss, H.W.; Haber, E.

1987-01-01

Indium-111 monoclonal antimyosin Fab scintigraphy was used to detect myocardial necrosis in 52 of 54 patients (96.3%) with acute myocardial infarction. Infarcts were visualized when coronary arteries were persistently occluded (n = 10), became patent after thrombolysis (n = 33), or became patent after spontaneous reperfusion (n = 7). Posteroinferolateral visualizations were obtained in two patients with clinical and enzymatic evidence of infarction but normal electrocardiograms. Of the two patients in whom no infarcts were visualized, one had an anterior myocardial infarct. This patient underwent successful thrombolytic therapy, with attendant minimization of creatine kinase release. The other patient had a small, nonreperfused inferior myocardial infarct. Five patients with a history of remote infarction and acute necrosis showed antimyosin uptake only in regions concordant with the acute episodes of infarction, and radiolabeled antimyosin Fab localized in neither old infarcts nor normal, noninfarcted myocardium. Antimyosin Fab scintigraphy, thus, appears to be a highly specific means of delineating necrotic myocardium, at least in this limited and selected group of patients

Diffuse corpus callosum infarction - Rare vascular entity with differing etiology.

Science.gov (United States)

Mahale, Rohan; Mehta, Anish; Buddaraju, Kiran; John, Aju Abraham; Javali, Mahendra; Srinivasa, Rangasetty

2016-01-15

Infarctions of the corpus callosum are rare vascular events. It is relatively immune to vascular insult because of its rich vascular supply from anterior and posterior circulations of brain. Report of 3 patients with largely diffuse acute corpus callosum infarction. 3 patients with largely diffuse acute corpus callosum infarction were studied and each of these 3 patients had 3 different aetiologies. The 3 different aetiologies of largely diffuse acute corpus callosum infarction were cardioembolism, tuberculous arteritis and takayasu arteritis. Diffuse corpus callosum infarcts are rare events. This case series narrates the three different aetiologies of diffuse acute corpus callosum infarction which is a rare vascular event. Copyright © 2015 Elsevier B.V. All rights reserved.

Elevated serum uric acid affects myocardial reperfusion and infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

Science.gov (United States)

Mandurino-Mirizzi, Alessandro; Crimi, Gabriele; Raineri, Claudia; Pica, Silvia; Ruffinazzi, Marta; Gianni, Umberto; Repetto, Alessandra; Ferlini, Marco; Marinoni, Barbara; Leonardi, Sergio; De Servi, Stefano; Oltrona Visconti, Luigi; De Ferrari, Gaetano M; Ferrario, Maurizio

2018-05-01

Elevated serum uric acid (eSUA) was associated with unfavorable outcome in patients with ST-segment elevation myocardial infarction (STEMI). However, the effect of eSUA on myocardial reperfusion injury and infarct size has been poorly investigated. Our aim was to correlate eSUA with infarct size, infarct size shrinkage, myocardial reperfusion grade and long-term mortality in STEMI patients undergoing primary percutaneous coronary intervention. We performed a post-hoc patients-level analysis of two randomized controlled trials, testing strategies for myocardial ischemia/reperfusion injury protection. Each patient underwent acute (3-5 days) and follow-up (4-6 months) cardiac magnetic resonance. Infarct size and infarct size shrinkage were outcomes of interest. We assessed T2-weighted edema, myocardial blush grade (MBG), corrected Thrombolysis in myocardial infarction Frame Count, ST-segment resolution and long-term all-cause mortality. A total of 101 (86.1% anterior) STEMI patients were included; eSUA was found in 16 (15.8%) patients. Infarct size was larger in eSUA compared with non-eSUA patients (42.3 ± 22 vs. 29.1 ± 15 ml, P = 0.008). After adjusting for covariates, infarct size was 10.3 ml (95% confidence interval 1.2-19.3 ml, P = 0.001) larger in eSUA. Among patients with anterior myocardial infarction the difference in delayed enhancement between groups was maintained (respectively, 42.3 ± 22.4 vs. 29.9 ± 15.4 ml, P = 0.015). Infarct size shrinkage was similar between the groups. Compared with non-eSUA, eSUA patients had larger T2-weighted edema (53.8 vs. 41.2 ml, P = 0.031) and less favorable MBG (MBG < 2: 44.4 vs. 13.6%, P = 0.045). Corrected Thrombolysis in myocardial infarction Frame Count and ST-segment resolution did not significantly differ between the groups. At a median follow-up of 7.3 years, all-cause mortality was higher in the eSUA group (18.8 vs. 2.4%, P = 0.028). eSUA may affect myocardial

Acute myocardial infarction

International Nuclear Information System (INIS)

RISCHPLER, Christoph

2016-01-01

Inflammatory processes after myocardial infarction have gained major interest in recent cardiovascular research. It is believed that not only the degree of cell recruitment to the heart plays a pivotal role in the quality of wound healing after myocardial infarction, but also the balance between different types or even subtypes of cells. It is also this balance which is thought to control key processes in tissue repair, such as apoptosis and neoangiogenesis. In this paper, we aim to review imaging strategies (with a special focus on nuclear molecular imaging strategies) that target cells and processes involved in postischemic inflammation and that have a high potential to be translated into clinic or that are already being used and evaluated in humans.

Right Ventricular Function After Acute Myocardial Infarction Treated With Primary Percutaneous Coronary Intervention : (from the Glycometabolic Intervention as Adjunct toPrimary Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction III Trial)

NARCIS (Netherlands)

Gorter, Thomas M; Lexis, Chris P H; Hummel, Yoran M; Lipsic, Erik; Nijveldt, Robin; Willems, Tineke P; van der Horst, Iwan C C; van der Harst, Pim; Melle, van J.P.; van Veldhuisen, Dirk J

2016-01-01

Right ventricular (RV) dysfunction is a powerful risk marker after acute myocardial infarction (MI). Primary percutaneous coronary intervention (PCI) has markedly reduced myocardial damage of the left ventricle, but reliable data on RV damage using cardiac magnetic resonance imaging (MRI) are

Evaluation of cat brain infarction model using microPET

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Lee, J. J.; Lee, D. S.; Kim, J. H.; Hwang, D. W.; Jung, J. G.; Lee, M. C [College of Medicine, Seoul National University, Seoul (Korea, Republic of); Lim, S. M [Korea Institute of Radiological and Medical Sciences, Seoul (Korea, Republic of)

2004-07-01

PET has some disadvantage in the imaging of small animal due to poor resolution. With the advance of microPET scanner, it is possible to image small animals. However, the image quality was not so much satisfactory as human image. As cats have relatively large sized brain, cat brain imaging was superior to mice or rat. In this study, we established the cat brain infarction model and evaluate it and its temporal change using microPET scanner. Two adult male cats were used. Anesthesia was done with xylazine and ketamine HCl. A burr hole was made at 1cm right lateral to the bregma. Collagenase type IV 10 ul was injected using 30G needle for 5 minutes to establish the infarction model. F-18 FDG microPET (Concorde Microsystems Inc., Knoxville. TN) scans were performed 1. 11 and 32 days after the infarction. In addition. 18F-FDG PET scans were performed using Gemini PET scanner (Philips medical systems. CA, USA) 13 and 47 days after the infarction. Two cat brain infarction models were established. The glucose metabolism of an infraction lesion improved with time. An infarction lesion was also distinguishable in the Gemini PET scan. We successfully established the cat brain infarction model and evaluated the infarcted lesion and its temporal change using F-18 FDG microPET scanner.

Evaluation of cat brain infarction model using microPET

International Nuclear Information System (INIS)

Lee, J. J.; Lee, D. S.; Kim, J. H.; Hwang, D. W.; Jung, J. G.; Lee, M. C; Lim, S. M

2004-01-01

PET has some disadvantage in the imaging of small animal due to poor resolution. With the advance of microPET scanner, it is possible to image small animals. However, the image quality was not so much satisfactory as human image. As cats have relatively large sized brain, cat brain imaging was superior to mice or rat. In this study, we established the cat brain infarction model and evaluate it and its temporal change using microPET scanner. Two adult male cats were used. Anesthesia was done with xylazine and ketamine HCl. A burr hole was made at 1cm right lateral to the bregma. Collagenase type IV 10 ul was injected using 30G needle for 5 minutes to establish the infarction model. F-18 FDG microPET (Concorde Microsystems Inc., Knoxville. TN) scans were performed 1. 11 and 32 days after the infarction. In addition. 18F-FDG PET scans were performed using Gemini PET scanner (Philips medical systems. CA, USA) 13 and 47 days after the infarction. Two cat brain infarction models were established. The glucose metabolism of an infraction lesion improved with time. An infarction lesion was also distinguishable in the Gemini PET scan. We successfully established the cat brain infarction model and evaluated the infarcted lesion and its temporal change using F-18 FDG microPET scanner

Coronary collateral circulation and its effect on myocardial infarction

International Nuclear Information System (INIS)

Fukuyama, Takaya; Ashihara, Toshiaki; Ogata, Ikuo

1995-01-01

The purpose of this study was to examine the influence of coronary collateral circulation, which grows after acute myocardial infarction (MI), on infarct size and prognosis. Study subjects were 47 patients who had arteriographic evidence of 99-100% constricture of the infarct-related artery approximately one month after the onset of the first MI. Coronary collateral circulation was analyzed by a four-point scoring (grade 0-3). Furthermore, the patients underwent thallium-201 myocardial imaging one month and two years after the onset to evaluate infarct size. Infarct size was analyzed using extent score (ES) and severity score (SS). ES tended to be decreased during chronic MI stage. Coronary collateral circulation was judged as grade 1 (n=9), grade 2 (n=12), and grade 3 (n=26). There was no difference in infarct size among the three groups. In groups of grades 1 and 2, there was no difference in ES and SS between acute and chronic MI stages. In the group of grade 3, however, ES decreased from 41% to 27% and SS decreased from 68% to 38%, showing remarkable decrease during chronic MI stage. Although coronary collateral circulation one month after the onset is not always responsible for infarct size during acute MI stage, it is considered rsponsible for inhibiting the remodeling of infarction through the long term process. (N.K.)

Myocardial infarction false alarm: initial electrocardiogram and cardiac enzymes.

Science.gov (United States)

Gupta, Esha Das; Sakthiswary, Rajalingham

2014-05-01

The objectives of this study were to determine the incidence of a myocardial infarction "false alarm" and evaluate the efficacy of the initial electrocardiogram and cardiac enzymes in diagnosing myocardial infarction in Malaysia. We recruited patients who were admitted with suspected myocardial infarction from June to August 2008. The medical records of these patients were reviewed for the initial electrocardiogram, initial cardiac enzyme levels (creatinine kinase-MB and troponin T), and the final diagnosis upon discharge. The subjects were stratified into 2 groups: true myocardial infarction, and false alarm. 125 patients were enrolled in this study. Following admission and further evaluation, the diagnosis was revised from myocardial infarction to other medical conditions in 48 (38.4%) patients. The sensitivity and specificity of the initial ischemic electrocardiographic changes were 54.5% and 70.8%, respectively. Raised cardiac enzymes had a sensitivity of 44.3% and specificity of 95.8%. A significant proportion of patients in Malaysia are admitted with a false-alarm myocardial infarction. The efficacy of the electrocardiogram in diagnosing myocardial infarction in Malaysia was comparable to the findings of Western studies, but the cardiac enzymes had a much lower sensitivity.

Adaptive partial median filter for early CT signs of acute cerebral infarction

International Nuclear Information System (INIS)

Lee, Yongbum; Tsai, Du-Yih; Takahashi, Noriyuki; Ishii, Kiyoshi

2007-01-01

Purpose: Detection of early CT signs of infarct in non- enhanced CT image is mandatory in patients with acute ischemic stroke. Loss of the gray-white matter interface at the lentiform nucleus or the insular ribbon has been an important early CT sign of acute cerebral infarction, which affects decisions on thrombolytic therapy. However, its detection is difficult, since the principal early CT sign is subtle hypoattenuation. An image processing method to reduce local noise with edges preserved was developed to improve infarct detection. Rationale: An adaptive partial median filter (APMF) was selected for this application, since the APMF can markedly improve the visibility of the normal gray-white matter interface. APMF should enhance the conspicuity of gray-white matter interface changes due to hypoattenuation that accompanies cerebral infarction. Method: In a criterion referenced performance study using simulated CT images with gray-white matter interfaces, a total of 14 conventional smoothing filters were also used for comparison to validate the usefulness of the proposed APMF. The APMF indicated the highest performance among the compared methods. Then, observer performance study by receiver operator characteristic (ROC) analysis was performed with 4 radiologist observers using a database with 18 abnormal and 33 normal head CT images. The average A z values of ROC curves for all radiologists increased from 0.876 without the APMF images to 0.926 with the APMF images, and this difference was statistically significant (P = 0.04). The results from the two observer performance studies demonstrated that APMF has significant potential to improve the diagnosis of acute cerebral infarction using non-enhanced CT images. (orig.)

A clinical study of brainstem infarction identified on magnetic resonance imaging

Energy Technology Data Exchange (ETDEWEB)

Watanabe, Masaki; Takahashi, Akira (Nagoya Univ. (Japan). Faculty of Medicine); Arahata, Yutaka; Motegi, Yoshimasa; Furuse, Masahiro

1993-04-01

We conducted a clinical study of 155 cases that were confirmed to have brainstem infarctions on MRI (T[sub 1]-weighted image showed a low signal and T[sub 2]-weighted image showed a high signal, measuring in excess of 2 x 2 mm). The majority of the brainstem infarction was located in the pontine base in 132 cases (85.2%). Of these, 19 cases had double lesions including infarctions in the pontine base. Second infarctions frequently occurred in the cerebral peduncle or medical medulla oblongata, unilateral to the pontine infarctions. In addition to 98 symptomatic cases, there were 57 cases of 'asymptomatic' brainstem infarction. They comprised 24 cases accompanying other symptomatic cerebrovascular diseases in the supratentorium and 33 cases of transient subjective complaints such as headache or vertigo-dizziness. Complication by supratentorial infarctions was significantly frequent in cases of brainstem infarction (p<0.001), 122 of 155 cases (78.7%), especially in the pontine base (88.6%); while in the control cases (without brainstem infarction) only 65 of 221 cases (29.4%). These findings are considered to show the widespread progress of arteriosclerosis in brainstem infarction, especially in ones in the pontine base. (author).

Relationship between blood viscosity and infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

Science.gov (United States)

Cecchi, Emanuele; Liotta, Agatina Alessandriello; Gori, Anna Maria; Valente, Serafina; Giglioli, Cristina; Lazzeri, Chiara; Sofi, Francesco; Gensini, Gian Franco; Abbate, Rosanna; Mannini, Lucia

2009-05-15

Previous studies explored the association between hemorheological alterations and acute myocardial infarction, pointing out the role of hematological components on microvascular flow. The aim of this study was to evaluate the association between blood viscosity and infarct size, estimated by creatine kinase (CK) peak activity and cardiac Troponin I (cTnI) peak concentration in ST-segment elevation myocardial infarction (STEMI) patients after primary percutaneous coronary intervention (PCI). The study population included 197 patients with diagnosis of STEMI undergoing PCI. Hemorheological studies were performed by assessing whole blood viscosity (measured at shear rates of 0.512 s(-1) and 94.5 s(-1)) and plasma viscosity using the Rotational Viscosimeter LS 30 and erythrocyte deformability index by Myrenne filtrometer. Significant correlations between CK peak activity, cTnI peak concentration, left ventricular ejection fraction and hemorheological variables were observed. At linear regression analysis (adjusted for age, gender, traditional cardiovascular risk factors, renal dysfunction, timeliness of reperfusion, pre-PCI TIMI flow, infarct location, multivessel disease and previous coronary artery disease) leukocytes and whole blood viscosity at 0.512 s(-1) and 94.5 s(-1) were independently and positively associated with infarct size. These results demonstrate a significant and independent association between hemorheology and infarct size in STEMI patients after PCI suggesting that blood viscosity, in a condition of low flow, might worsen myocardial perfusion leading to an increased infarct size. The measurement of whole blood viscosity in STEMI patients could help to identify those who may benefit from new therapeutic strategies.

Near-infrared diffuse reflectance imaging of infarct core and peri-infarct depolarization in a rat middle cerebral artery occlusion model

Science.gov (United States)

Kawauchi, Satoko; Nishidate, Izumi; Nawashiro, Hiroshi; Sato, Shunichi

2014-03-01

To understand the pathophysiology of ischemic stroke, in vivo imaging of the brain tissue viability and related spreading depolarization is crucial. In the infarct core, impairment of energy metabolism causes anoxic depolarization (AD), which considerably increases energy consumption, accelerating irreversible neuronal damage. In the peri-infarct penumbra region, where tissue is still reversible despite limited blood flow, peri-infarct depolarization (PID) occurs, exacerbating energy deficit and hence expanding the infarct area. We previously showed that light-scattering signal, which is sensitive to cellular/subcellular structural integrity, was correlated with AD and brain tissue viability in a rat hypoxia-reoxygenation model. In the present study, we performed transcranial NIR diffuse reflectance imaging of the rat brain during middle cerebral artery (MCA) occlusion and examined whether the infarct core and PIDs can be detected. Immediately after occluding the left MCA, light scattering started to increase focally in the occlusion site and a bright region was generated near the occlusion site and spread over the left entire cortex, which was followed by a dark region, showing the occurrence of PID. The PID was generated repetitively and the number of times of occurrence in a rat ranged from four to ten within 1 hour after occlusion (n=4). The scattering increase in the occlusion site was irreversible and the area with increased scattering expanded with increasing the number of PIDs, indicating an expansion of the infarct core. These results suggest the usefulness of NIR diffuse reflectance signal to visualize spatiotemporal changes in the infarct area and PIDs.

Echocardiographic Diagnostics of Myocardial Infarction in Newborns

Directory of Open Access Journals (Sweden)

G. V. Revunenkov

2015-01-01

Full Text Available Early and correct diagnostics of myocardial infarction in newborns is impossible without modern instrumental methods, among which echocardiography is the leading one. Hypokinesia, akinesia or dyskinesia of local segments of the heart ventricular wall is determined with echocardiography. We examined a 3-days-old baby with circulatory failure requiring cardiotonic support. On auscultation there was a heart murmur. It was an intracardiac conduction disoder and infarction-like changes on ECG, however, a convincing evidence to interpret the patient’s condition as myocardial infarction has not been received. Therefore, it was decided to conduct echocardiography. According to the results of echocardiography the presence of hyperechogenic diskinetic locus in the apical segment of the right ventricle (post-infarction scar, a local pericardial effusion in the same projection, hyperechogenic movable mass (thrombus in the apical segment of the right ventricle were determined that together with the results of the ECG allowed us to set diagnosis myocardial infarction. Transthoracic echocardiography is one of highly informative methods; the data obtained allowed to correctly interpret the clinical picture of heart failure and to reveal the cause of the patien’st dependance on cardiotonic support.

Proton NMR imaging in experimental ischemic infarction

International Nuclear Information System (INIS)

Buonanno, F.S.; Pykett, I.L.; Brady, T.J.; Vielma, J.; Burt, C.T.; Goldman, M.R.; Hinshaw, W.S.; Pohost, G.M.; Kistler, J.P.

1983-01-01

Proton nuclear magnetic resonance (NMR) images depict the distribution and concentration of mobile protons modified by the relaxation times T1 and T2. Using the steady-state-free-precession (SSFP) technique, serial coronal images were obtained sequentially over time in laboratory animals with experimental ischemic infarction. Image changes were evident as early as 2 hours after carotid artery ligation, and corresponded to areas of ischemic infarction noted pathologically. Resulting SSFP images in experimental stroke are contrasted to inversion-recovery NMR images in an illustrative patient with established cerebral infarction. Bulk T1 and T2 measurements were made in vitro in three groups of gerbils: normal, those with clinical evidence of infarction, and those clinically normal after carotid ligature. Infarcted hemispheres had significantly prolonged T1 and T2 (1.47 +/- .12 sec, 76.0 +/- 9.0 msec, respectively) when compared to the contralateral hemisphere (T1 . 1.28 +/- .05 sec, T2 . 58.7 +/- 3.9 msec) or to the other two groups. These data suggest that changes in NMR parameters occur and can be detected by NMR imaging as early as two hours after carotid artery ligation

A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group

DEFF Research Database (Denmark)

Køber, L; Torp-Pedersen, C; Carlsen, J E

1995-01-01

myocardial infarctions confirmed by enzyme studies. A total of 2606 patients had echocardiographic evidence of left ventricular systolic dysfunction (ejection fraction, ....86; 95 percent confidence interval, 0.66 to 1.13; P = 0.29). CONCLUSIONS. Long-term treatment with trandolapril in patients with reduced left ventricular function soon after myocardial infarction significantly reduced the risk of overall mortality, mortality from cardiovascular causes, sudden death...

[Study of cerebellar infarction with isolated vertigo].

Science.gov (United States)

Utsumi, Ai; Enomoto, Hiroyuki; Yamamoto, Kaoru; Kimura, Yu; Koizuka, Izumi; Tsukuda, Mamoru

2010-07-01

Isolated vertigo is generally attributed to labyrinthine disease, but may also signal otherwise asymptomatic cerebellar infarction. Of 309 subjects admitted between April 2004 and March 2009 for the single symptom of acute vertigo initially thought to be labyrinthine, four were found to have cerebellar infarction of the posterior inferior cerebellar artery area (PICA). All were over 60 years old and had risk factors including hypertension, diabetes mellitus, arrhythmia, and/or hyperlipidemia. Two had trunk ataxia, with magnetic resonance imaging (MRI) showing infarction within a few days. The other two could walk without apparent trunk ataxia, however, it took 4 to 7 days to find the infarction, mainly through neurological, neurootological, and MRI findings. Neurologically, astasia, dysbasia or trunk ataxia were important signs. Neurootologically, nystagmus and electronystagmographic testing involving eye tracking, saccade, and optokinetic patttens were useful.

Measurement of infarct size and percentage myocardium infarcted in a dog preparation with single photon-emission computed tomography, thallium-201, and indium 111-monoclonal antimyosin Fab

International Nuclear Information System (INIS)

Johnson, L.L.; Lerrick, K.S.; Coromilas, J.

1987-01-01

Single photon-emission tomography (SPECT) and indium 111-labeled monoclonal antimyosin Fab fragments were used to measure myocardial infarct size in 12 dogs, six subjected to balloon catheter-induced coronary artery occlusion for 6 hr (late reperfusion) and six subjected to occlusion with reperfusion at 2 hr (early reperfusion). Tomographic imaging was performed 24 hr after the intravenous injection of labeled Fab fragments with the use of a dual-head SPECT camera with medium-energy collimators. Immediately after the first tomographic scan, thallium-201 was injected into nine of 12 dogs and imaging was repeated. Estimated infarct size in grams was calculated from transaxially reconstructed, normalized, and background-corrected indium SPECT images with the use of a threshold technique for edge detection. Estimated noninfarcted myocardium in grams was calculated from obliquely reconstructed thallium SPECT images by a similar method. The animals were killed and infarct size in grams and true infarct size as a percentage of total left ventricular myocardial volume were measured by triphenyl tetrazolium chloride staining. Estimated infarct size from indium SPECT images showed an excellent correlation with true infarct size (r = .95, SEE = 4.1 g). Estimated percentage myocardium infarcted was calculated by dividing estimated infarct size from indium images by the sum of estimated infarct size plus estimated noninfarcted myocardium obtained from thallium images. Correlation between the estimated percentage of myocardium infarcted and true percentage of myocardium infarcted was excellent

Depressive disorder and gastrointestinal dysfunction after myocardial infarct are associated with abnormal tryptophan-5-hydroxytryptamine metabolism in rats.

Science.gov (United States)

Lu, Xiaofang; Wang, Yuefen; Liu, Chunyan; Wang, Yangang

2017-01-01

In this study, we investigated the relationship between tryptophan-5-hydroxytryptamine metabolism, depressive disorder, and gastrointestinal dysfunction in rats after myocardial infarction. Our goal was to elucidate the physiopathologic bases of somatic/psychiatric depression symptoms after myocardial infarction. A myocardial infarction model was established by permanent occlusion of the left anterior descending coronary artery. Depression-like behavior was evaluated using the sucrose preference test, open field test, and forced swim test. Gastric retention and intestinal transit were detected using the carbon powder labeling method. Immunohistochemical staining was used to detect indoleamine 2,3-dioxygenase expression in the hippocampus and ileum. High-performance liquid chromatography with fluorescence and ultraviolet detection determined the levels of 5-hydroxytryptamine, its precursor tryptophan, and its metabolite 5-hydroxyindoleacetic acid in the hippocampus, distal ileum, and peripheral blood. All data were analyzed using one-way analyses of variance. Three weeks after arterial occlusion, rats in the model group began to exhibit depression-like symptoms. For example, the rate of sucrose consumption was reduced, the total and central distance traveled in the open field test were reduced, and immobility time was increased, while swimming, struggling and latency to immobility were decreased in the forced swim test. Moreover, the gastric retention rate and gastrointestinal transit rate were increased in the model group. Expression of indoleamine 2,3-dioxygenase was increased in the hippocampus and ileum, whereas 5-hydroxytryptamine metabolism was decreased, resulting in lower 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels in the hippocampus and higher levels in the ileum. Depressive disorder and gastrointestinal dysfunction after myocardial infarction involve abnormal tryptophan-5-hydroxytryptamine metabolism, which may explain the somatic, cognitive

Depressive disorder and gastrointestinal dysfunction after myocardial infarct are associated with abnormal tryptophan-5-hydroxytryptamine metabolism in rats.

Directory of Open Access Journals (Sweden)

Xiaofang Lu

Full Text Available In this study, we investigated the relationship between tryptophan-5-hydroxytryptamine metabolism, depressive disorder, and gastrointestinal dysfunction in rats after myocardial infarction. Our goal was to elucidate the physiopathologic bases of somatic/psychiatric depression symptoms after myocardial infarction. A myocardial infarction model was established by permanent occlusion of the left anterior descending coronary artery. Depression-like behavior was evaluated using the sucrose preference test, open field test, and forced swim test. Gastric retention and intestinal transit were detected using the carbon powder labeling method. Immunohistochemical staining was used to detect indoleamine 2,3-dioxygenase expression in the hippocampus and ileum. High-performance liquid chromatography with fluorescence and ultraviolet detection determined the levels of 5-hydroxytryptamine, its precursor tryptophan, and its metabolite 5-hydroxyindoleacetic acid in the hippocampus, distal ileum, and peripheral blood. All data were analyzed using one-way analyses of variance. Three weeks after arterial occlusion, rats in the model group began to exhibit depression-like symptoms. For example, the rate of sucrose consumption was reduced, the total and central distance traveled in the open field test were reduced, and immobility time was increased, while swimming, struggling and latency to immobility were decreased in the forced swim test. Moreover, the gastric retention rate and gastrointestinal transit rate were increased in the model group. Expression of indoleamine 2,3-dioxygenase was increased in the hippocampus and ileum, whereas 5-hydroxytryptamine metabolism was decreased, resulting in lower 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels in the hippocampus and higher levels in the ileum. Depressive disorder and gastrointestinal dysfunction after myocardial infarction involve abnormal tryptophan-5-hydroxytryptamine metabolism, which may explain the

Effects of buprenorphine and meloxicam analgesia on induced cerebral ischemia in C57BL/6 male mice

DEFF Research Database (Denmark)

Jacobsen, Kirsten R; Fauerby, Natasha; Raida, Zindy

2013-01-01

Laboratory mice constitute an extensively used model to study the pathologic and functional outcomes of cerebral ischemic stroke. The middle cerebral artery occlusion (MCAO) model requires surgical intervention, which potentially can result in postsurgical pain and stress. In the present study, we...... investigated whether buprenorphine and meloxicam, at clinically relevant doses provided pain relief without altering infarct volume in male C57BL/6 mice. Common known side-effects of buprenorphine, including decreased food consumption, were noted after surgery in buprenorphine-treated mice, but these effects...

Omental infarction in an obese 10-year-old boy

Directory of Open Access Journals (Sweden)

Katerina Kambouri

2011-09-01

Full Text Available Primary omental infarction (POI has a low incidence worldwide, with most cases occurring in adults. This condition is rarely considered in the differential diagnosis of acute abdominal pain in childhood. Herein, we present a case of omental infarction in an obese 10-year-old boy who presented with acute abdominal pain in the right lower abdomen. The ultrasound (US examination did not reveal the appendix but showed secondary signs suggesting acute appendicitis. The child was thus operated on under the preoperative diagnosis of acute appendicitis but the intraoperative finding was omental infarct. Since the omental infarct as etiology of acute abdominal pain is uncommon, we highlight some of the possible etiologies and emphasize the importance of accurate diagnosis and appropriate treatment of omental infarction.

Pathological Laughter as a Symptom of Midbrain Infarction

Science.gov (United States)

Dabby, Ron; Watemberg, Nathan; Lampl, Yair; Eilam, Anda; Rapaport, Abraham; Sadeh, Menachem

2004-01-01

Pathological laughter is an uncommon symptom usually caused by bilateral, diffuse cerebral lesions. It has rarely been reported in association with isolated cerebral lesions. Midbrain involvement causing pathological laughter is extremely unusual. We describe three patients who developed pathological laughter after midbrain and pontine-midbrain infarction. In two patients a small infarction in the left paramedian midbrain was detected, whereas the third one sustained a massive bilateral pontine infarction extending to the midbrain. Laughter heralded stroke by one day in one patient and occurred as a delayed phenomenon three months after stroke in another. Pathological laughter ceased within a few days in two patients and was still present at a two year follow-up in the patient with delayed-onset laughter. Pathological laughter can herald midbrain infarction or follow stroke either shortly after onset of symptoms or as a delayed phenomenon. Furthermore, small unilateral midbrain infarctions can cause this rare complication. PMID:15706050

Determination of infarct size of acute myocardial infarction in dogs by magnetic resonance imaging and gadolinium-DTPA: Comparison with indium-111 antimyosin imaging

International Nuclear Information System (INIS)

Nishimura, T.; Yamada, Y.; Hayashi, M.; Kozuka, T.; Nakatani, T.; Noda, H.; Takano, H.

1989-01-01

Acute myocardial infarctions were produced in nine dogs by ligation of the left anterior descending coronary artery. Twenty-four hours after ligation, 0.5 mM/kg of gadolinium (Gd)-DTPA was injected intravenously, followed by cardiectomy 30 min later. Indium-111 antimyosin was administered intravenously 6 hr before cardiectomy to compare the infarct size with Gd-DTPA contrast enhancement. Areas of Gd-DTPA contrast enhancement were closely correlated with those of indium-111 antimyosin uptake (r = .86), although the former showed slightly greater than the latter. Partial and complete enhancements were observed in three and six dogs, respectively. In the T1 and T2 maps, T1 relaxation times of the infarcted area showed greater T1 shortening compared with normal myocardium, whereas T2 relaxation times were not different between infarcted and normal myocardium. Thus, Gd-DTPA showed significant contrast enhancement of the infarcted area because of greater T1 shortening and the extent of Gd-DTPA contrast enhancement expressed the infarct size precisely

Ventricular Septal Dissection Complicating Inferior Wall Myocardial Infarction

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Lindsey Kalvin

2017-01-01

Full Text Available Postmyocardial infarction ventricular septal defect is an increasingly rare mechanical complication of acute myocardial infarction. We present a case of acute myocardial infarction from right coronary artery occlusion that developed hypotension and systolic murmur 12 hours after successful percutaneous coronary intervention. Although preoperative imaging suggested a large ventricular septal defect and a pseudoaneurysm, intraoperative findings concluded a serpiginous dissection of the ventricular septum. The imaging technicalities are discussed.

PSYCHOLOGICAL REACTIONS AND HEALTH BEHAVIOR FOLLOWING ACUTE MYOCARDIAL INFARCTION

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Tatjana Milenković

2011-06-01

rehabilitation of patients after myocardial infarction there should be considerable psychoeducation of patients with the aim to reduce their risk health behavior.

Bilateral orbital bone infarction in sickle-cell disease.

Science.gov (United States)

Ghafouri, Roya H; Lee, Irene; Freitag, Suzanne K; Pira, Tony N

2011-01-01

This is a case of a 2-year-old boy with sickle cell disease who presented with bilateral eyelid swelling, limited extraocular motility, and lateral subperiosteal fluid collection associated with bilateral lateral orbital wall infarctions on MRI. The patient was managed medically with intravenous fluids, analgesics, broad-spectrum antibiotics, systemic steroids, and clinically improved. Patients with sickle cell disease are susceptible to infarction of the orbital bones during vaso-occlusive crises. Orbital wall infarction can lead to acute proptosis and restricted extraocular motility. Orbital wall infarction should be considered in sickle cell patients with orbital diseases so that appropriate treatment can be instituted promptly to prevent the serious sequelae of orbital compression syndrome.

Role of adenosine as adjunctive therapy in acute myocardial infarction.

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Forman, Mervyn B; Stone, Gregg W; Jackson, Edwin K

2006-01-01

Although early reperfusion and maintained patency is the mainstay therapy for ST elevation myocardial infarction, experimental studies demonstrate that reperfusion per se induces deleterious effects on viable ischemic cells. Thus "myocardial reperfusion injury" may compromise the full potential of reperfusion therapy and may account for unfavorable outcomes in high-risk patients. Although the mechanisms of reperfusion injury are complex and multifactorial, neutrophil-mediated microvascular injury resulting in a progressive decrease in blood flow ("no-reflow" phenomenon) likely plays an important role. Adenosine is an endogenous nucleoside found in large quantities in myocardial and endothelial cells. It activates four well-characterized receptors producing various physiological effects that attenuate many of the proposed mechanisms of reperfusion injury. The cardio-protective effects of adenosine are supported by its role as a mediator of pre- and post-conditioning. In experimental models, administration of adenosine in the peri-reperfusion period results in a marked reduction in infarct size and improvement in ventricular function. The cardioprotective effects in the canine model have a narrow time window with the drug losing its effect following three hours of ischemia. Several small clinical studies have demonstrated that administration of adenosine with reperfusion therapy reduces infarct size and improves ventricular function. In the larger AMISTAD and AMISTAD II trials a 3-h infusion of adenosine as an adjunct to reperfusion resulted in a striking reduction in infarct size (55-65%). Post hoc analysis of AMISTAD II showed that this was associated with significantly improved early and late mortality in patients treated within 3.17 h of symptoms. An intravenous infusion of adenosine for 3 h should be considered as adjunctive therapy in high risk-patients undergoing reperfusion therapy.

The Effects of Inhalation Aromatherapy on Anxiety in Patients With Myocardial Infarction: A Randomized Clinical Trial

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Najafi, Zahra; Taghadosi, Mohsen; Sharifi, Khadijeh; Farrokhian, Alireza; Tagharrobi, Zahra

2014-01-01

Background: Anxiety is an important mental health problem in patients with cardiac disease. Anxiety reduces patients’ quality of life and increases the risk of different cardiac complications. Objectives: The aim of this study was to investigate the effects of inhalation aromatherapy on anxiety in patients with myocardial infarction. Patients and Methods: This was a randomized clinical trial conduced on 68 patients with myocardial infarction hospitalized in coronary care units of a large-scale teaching hospital affiliated to Kashan University of Medical Sciences, Kashan, Iran in 2013. By using the block randomization technique, patients were randomly assigned to experimental (33 patients receiving inhalation aromatherapy with lavender aroma twice a day for two subsequent days) and control (35 patients receiving routine care of study setting including no aromatherapy) groups. At the beginning of study and twenty minutes after each aromatherapy session, anxiety state of patients was assessed using the Spielberger’s State Anxiety Inventory. Data was analyzed using SPSS v. 16.0. We used Chi-square, Fisher’s exact, independent-samples T-test and repeated measures analysis of variance to analyze the study data. Results: The study groups did not differ significantly regarding baseline anxiety mean and demographic characteristics. However, after the administration of aromatherapy, anxiety mean in the experimental group was significantly lower than the control group. Conclusions: Inhalation aromatherapy with lavender aroma can reduce anxiety in patients with myocardial infarction. Consequently, healthcare providers, particularly nurses, can use this strategy to improve postmyocardial infarction anxiety management. PMID:25389481

Clinical predictors of lacunar syndrome not due to lacunar infarction

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Comes Emili

2010-05-01

Full Text Available Background Lacunar syndrome not due to lacunar infarct is poorly characterised. This single centre, retrospective study was conducted to describe the clinical characteristics of patients with lacunar syndrome not due to lacunar infarct and to identify clinical predictors of this variant of lacunar stroke. Methods A total of 146 patients with lacunar syndrome not due to lacunar infarction were included in the "Sagrat Cor Hospital of Barcelona Stroke Registry" during a period of 19 years (1986-2004. Data from stroke patients are entered in the stroke registry following a standardized protocol with 161 items regarding demographics, risk factors, clinical features, laboratory and neuroimaging data, complications and outcome. The characteristics of these 146 patients with lacunar syndrome not due to lacunar infarct were compared with those of the 733 patients with lacunar infarction. Results Lacunar syndrome not due to lacunar infarct accounted for 16.6% (146/879 of all cases of lacunar stroke. Subtypes of lacunar syndromes included pure motor stroke in 63 patients, sensorimotor stroke in 51, pure sensory stroke in 14, atypical lacunar syndrome in 9, ataxic hemiparesis in 5 and dysarthria-clumsy hand in 4. Valvular heart disease, atrial fibrillation, sudden onset, limb weakness and sensory symptoms were significantly more frequent among patients with lacunar syndrome not due to lacunar infarct than in those with lacunar infarction, whereas diabetes was less frequent. In the multivariate analysis, atrial fibrillation (OR = 4.62, sensorimotor stroke (OR = 4.05, limb weakness (OR = 2.09, sudden onset (OR = 2.06 and age (OR = 0.96 were independent predictors of lacunar syndrome not due to lacunar infarct. Conclusions Although lacunar syndromes are highly suggestive of small deep cerebral infarctions, lacunar syndromes not due to lacunar infarcts are found in 16.6% of cases. The presence of sensorimotor stroke, limb weakness and sudden onset in a patient

Renal infarction: CT diagnosis and correlation between CT findings and etiologies

International Nuclear Information System (INIS)

Wong, W.S.; Moss, A.A.; Federle, M.P.; Cochran, S.T.; London, S.S.

1984-01-01

The CT scans and the clinical records of 12 patients who had renal infarction were reviewed. The renal infarcts were classified as either focal or global. The CT findings were correlated with the etiologies of renal infarction. Embolism was the most common cause of renal infarcts that were multifocal with involvement of both kidneys. Trauma caused a unilateral global type of infract. A case of sickle cell anemia presented with multiple ''slit-like'' focal infarcts and enlarged kidneys. Forty-seven per cent of infarcts demonstrated the cortical rim sign, 11% were acapsular fluid collection, and 6% had an abnormally thickened renal fascia

Acute and chronic myocardial infarction in a pig model: Utility of multi-slice cardiac computed tomography in assessing myocardial viability and infarct parameters

International Nuclear Information System (INIS)

Qu Xinkai; Fang Weiyi; Ye Jianding; Koh, Angela S.; Xu Yingjia; Guan Shaofeng; Li Ruogu; Shen Yan

2012-01-01

Objectives: The aim of this study was to determine the feasibility of multi-slice computed tomography (MSCT) biphasic imaging in assessing myocardial viability and infarct parameters in both acutely and chronically infarcted pig models. Materials and methods: Seven pigs underwent ligation of the distal left anterior descending artery. Imaging was performed on the day of infarction and 3 months post-infarct, with contrast infusion followed by MSCT scan acquisition at different time-points. Left ventricular ejection fractions (LVEFs) were obtained by left ventriculography (LVG) after 3 months. Infarcted locations found using MSCT were compared with those obtained using SPECT. Infarcted areas were also analysed histopathologically and compared with the findings from MSCT. Results: Chronic phase images had perfusion defects with lower CT values relative to normal myocardium (43 ± 10 HU vs. 156 ± 13 HU, p = 0.001) on the early images but no residual defects on delayed images. However, we found hyperenhancing regions on delayed images (244 ± 20 HU vs. 121 ± 25 HU, p = 0.001), and good correlation between MSCT- and LVG-derived LVEFs (60.56 ± 7.56%). The areas identified by MSCT corresponded to the location of 201 Tl SPECT-/pathologic staining-derived regions in all models. Infarct size was in good agreement with MSCT and pathological analyses of chronic phase models. Conclusions: Necrotic myocardium in different stages after infarction could be qualitatively and quantitatively assessed using MSCT biphasic imaging, as could the status of microcirculation formation. MSCT-measured LVEFs matched well with other modalities, and hence MSCT is a useful tool in assessing post-infarct cardiac function.

Bilateral optical nerve atrophy secondary to lateral occipital lobe infarction.

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Mao, Junfeng; Wei, Shihui

2013-06-01

To report a phenomenon of optical nerve atrophy secondary to lateral occipital lobe infarction. Two successive patients with unilateral occipital lobe infarction who experienced bilateral optical nerve atrophy during the follow-up underwent cranial imaging, fundus photography, and campimetry. Each patient was diagnosed with occipital lobe infarction by cranial MRI. During the follow-up, a bilateral optic atrophy was revealed, and campimetry showed a right homonymous hemianopia of both eyes with concomitant macular division. Bilateral optic atrophy was related to occipital lobe infarction, and a possible explanation for the atrophy was transneuronal degeneration caused by occipital lobe infarction.

Factors associated with the misdiagnosis of cerebellar infarction.

Science.gov (United States)

Masuda, Yoko; Tei, Hideaki; Shimizu, Satoru; Uchiyama, Shinichiro

2013-10-01

Cerebellar infarction is easily misdiagnosed or underdiagnosed. In this study, we investigated factors leading to misdiagnosis of cerebellar infarction in patients with acute ischemic stroke. Data on neurological and radiological findings from 114 consecutive patients with acute cerebellar infarction were analyzed. We investigated factors associated with misdiagnosis from the data on clinical findings. Thirty-two (28%) patients were misdiagnosed on admission. Misdiagnosis was significantly more frequent in patients below 60 years of age and in patients with vertebral artery dissection, and significantly less frequent in patients with dysarthria. It tended to be more frequent in patients with the medial branch of posterior inferior cerebellar artery territory infarction, and infrequent in patients with the medial branch of the superior cerebellar artery territory infarction. Thirty out of 32 (94%) misdiagnosed patients were seen by physicians that were not neurologists at the first visit. Twenty-four of 32 (75%) misdiagnosed patients were screened only by brain CT. However, patients were not checked by brain MRI or follow-up CT until their conditions worsened. Patients below 60 years of age and patients with vertebral artery dissection are more likely to have a cerebellar infarction misdiagnosed by physicians other than neurologists. Copyright © 2013 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Unexpected Coexisting Myocardial Infarction Detected by Delayed Enhancement MRI

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Edouard Gerbaud

2009-01-01

Full Text Available We report a case of an unexpected coexisting anterior myocardial infarction detected by delayed enhancement MRI in a 41-year-old man following a presentation with a first episode of chest pain during inferior acute myocardial infarction. This second necrotic area was not initially suspected because there were no ECG changes in the anterior leads and the left descending coronary artery did not present any significant stenoses on emergency coronary angiography. Unrecognised myocardial infarction may carry important prognostic implications. CMR is currently the best imaging technique to detect unexpected infarcts.

Brain infarcts due to scorpion stings in children: MRI

International Nuclear Information System (INIS)

Fernandez-Bouzas, A.; Ballesteros-Maresma, A.; Morales-Resendiz, M.L.; Llamas-Ibarra, F.; Martinez-Lopez, M.

2000-01-01

We report two children with severe neurological complications after having been stung by a scorpion. Clinical and MRI findings suggested brain infarcts. The lesions seen were in pons in one child and the right hemisphere in the other. The latter also showed possible hyperemia in the infarcted area. No vascular occlusions were observed and we therefore think the brain infarcts were a consequence of the scorpion sting. The cause of the infarct may be hypotension, shock or depressed left ventricular function, all of which are frequent in severe poisoning by scorpion sting. (orig.)

Prognostic relevance of PCI-related myocardial infarction

NARCIS (Netherlands)

Woudstra, Pier; Grundeken, Maik J.; van de Hoef, Tim P.; Wallentin, Lars; Fox, Keith A.; de Winter, Robbert J.; Damman, Peter

2013-01-01

Procedure-related myocardial infarction (pMI) is directly associated with a coronary revascularization procedure, such as percutaneous coronary intervention (PCI) or CABG surgery. In contrast to spontaneous myocardial infarction (MI), the prognostic relevance of pMI is the subject of ongoing debate.

Time course of neuroprotection induced by in vivo normobaric hyperoxia preconditioning and angiogenesis factors

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Meisam Shahhoseini

2017-01-01

Full Text Available Objective(s:Every year, a large number of people lose their lives due to stroke. Stroke is the second leading cause of death worldwide. Surprisingly, recent studies have shown that preconditioning with hyperoxia (HO increases tissue tolerance to ischemia, ultimately reducing damages caused by stroke. Addressed in this study are beneficial contributions from HO preconditioning into reduced harm to be incurred by the attack, as well as its effect on the expression levels of vascular endothelial growth factor (VEGF and endostatin. Materials and Methods: A set of experiments was conducted where a number of rats were divided into three groups. The animals in the first group received 90% oxygen for 4 hr a day, for 6 days. The second group was housed in room air and the third group was a sham (surgical stress. After 60 min of ischemia, 24 hr blood flow, neurological deficit score (NDS and infarct volume (IV in the group MCAO (Middle Cerebral Artery Occlusion were investigated. Immediately following a 48 hr HO pre-treatment, sampling was performed to measure the expression levels of VEGF and endostatin. Results: Preconditioning with alternating HO led to reduced infarct volume and NDS. Moreover, pre-treatment with HO resulted in increased VEGF expression while decreasing endostatin. Conclusion: Although further studies are deemed necessary to clarify the mechanisms of ischemic tolerance, apparently, somewhat intermittent hyperoxia can be associated with positive impacts by increasing VEGF and decreasing expression of endostatin.

Benefits of lifelong exercise training on left ventricular function after myocardial infarction.

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Maessen, Martijn Fh; Eijsvogels, Thijs Mh; Stevens, Guus; van Dijk, Arie Pj; Hopman, Maria Te

2017-11-01

Background Endurance exercise training induces cardio-protective effects, but athletes are not exempted from a myocardial infarction. Evidence from animal studies suggests that exercise training attenuates pathological left ventricular remodelling following myocardial infarction. We tested the hypothesis that lifelong exercise training is related to attenuated pathological left ventricular remodelling after myocardial infarction as evidenced by better left ventricular systolic function in veteran athletes compared to sedentary peers. Design This was a cross-sectional study. Methods Sixty-five males (60 ± 6 years) were included and allocated to four groups based on lifelong exercise training volumes: (a) athletes ( n = 18), (b) post-myocardial infarction athletes (athletes + myocardial infarction, n = 20), (c) sedentary controls ( n = 13), and (d) post-myocardial infarction controls (sedentary controls + myocardial infarction, n = 14). Athletes were lifelong (≥20 years) highly physically active (≥30 metabolic equivalent of task (MET)-h/week), whereas sedentary controls did not meet the exercise guidelines (creatine-kinase, creatinine, aspartate transaminase and lactate dehydrogenase) following myocardial infarction and infarct location did not differ between athletes + myocardial infarction and sedentary controls + myocardial infarction. Left ventricular ejection fraction was significantly higher in athletes (61% ± 4), athletes + myocardial infarction (58% ± 4) and sedentary controls (57% ± 6) compared to sedentary controls + myocardial infarction (51% ± 7; p athletes (-19% (-21% to -17%), athletes + myocardial infarction (-16% (-20% to -12%)), and sedentary controls (-15% (-18% to -14%) compared to sedentary controls + myocardial infarction (-13% (-15% to -8%), p athletes.

The effect of optimal medical therapy on 1-year mortality after acute myocardial infarction.

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Bramlage, P; Messer, C; Bitterlich, N; Pohlmann, C; Cuneo, A; Stammwitz, E; Tebbenjohanns, J; Gohlke, H; Senges, J; Tebbe, U

2010-04-01

Five drug classes have been shown to improve the prognosis of acute myocardial infarction in clinical trials: aspirin, beta-blockers, statins, renin angiotensin system (RAS) blockers and thienopyridines. We aimed to assess whether the benefits of combining these drugs (termed optimal medical therapy, OMT), will result in a reduction of mortality in clinical practice. Nationwide registry Hospitals with a cardiology unit or internal medicine department. 5353 patients with acute myocardial infarction. At hospital discharge 89% received aspirin, 90% beta-blockers, 84% statins, 81% RAS blockers, 70% a thienopyridine and 46.2% OMT. Pharmacotherapy OR with 95% CI for mortality from myocardial infarction were calculated and adjusted for patient risk at baseline. Total mortality was reduced by 74% in patients receiving OMT (adj OR 0.26; 95% CI 0.18 to 0.38) versus patients receiving one or no drug. This was consistent in subgroups defined by STEMI/NSTEMI, diabetes and gender. Mortality was also reduced in patients receiving 2-4 drugs (adj OR 0.49; 95% CI 0.35 to 0.68), diabetic patients being the only subgroup with no significant effect. Analyses on the relative importance of either component revealed that withdrawal of beta-blockers (adj OR 0.63; 95% CI 0.34 to 1.16) and/or a combination of aspirin/clopidogrel (adj OR 0.59; 95% CI 0.20 to 1.17) abolished the risk reduction conferred by OMT. OMT over 1 year was associated with a significantly lower mortality of patients with acute myocardial infarction in clinical practice. However OMT is provided to less than half of eligible patients leaving room for substantial improvement.

High-dose fasudil preserves postconditioning against myocardial infarction under hyperglycemia in rats: role of mitochondrial KATP channels

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Ichinomiya Taiga

2012-03-01

Full Text Available Abstract Background The current study was carried out to determine whether fasudil hydrochloride (fasudil, a Rho-kinase inhibitor, has myocardial postconditioning (PostC activity under hyperglycemia as well as normoglycemia, and if so, whether the effects could be mediated by mitochondrial ATP-sensitive potassium (m-KATP channels. Methods Male Sprague-Dawley rats were anesthetized with sodium pentobarbital. After opening the chest, all rats underwent 30-min coronary artery occlusion followed by 2-h reperfusion. The rats received low-dose (0.15 mg/kg or high-dose (0.5 mg/kg fasudil or diazoxide, an m-KATP channel opener, at 10 mg/kg, just before reperfusion under normoglycemic or hyperglycemic conditions. In another group, rats received 5-hydroxydecanoic acid (5HD, an m-KATP channel blocker, at 10 mg/kg, before high-dose fasudil. Myocardial infarct size was expressed as a percentage of area at risk (AAR. Results Under normoglycemia, low-dose and high-dose fasudil and diazoxide reduced myocardial infarct size (23 ± 8%, 21 ± 9% and 21 ± 10% of AAR, respectively compared with that in the control (42 ± 7%. Under hyperglycemia, low-dose fasudil (40 ± 11% and diazoxide (44 ± 14% could not exert this beneficial effect, but high-dose fasudil reduced myocardial infarct size in the same manner as under normoglycemia (21 ± 13%. 5HD prevented fasudil-induced reduction of myocardial infarct size (42 ± 13%. Conclusion Fasudil induces PostC against myocardial infarction via activation of m-KATP channels in the rat. Although hyperglycemia attenuates the PostC, high-dose fasudil can restore cardioprotection.

Evaluation of thallium redistribution in infarcted area in accordance with time interval from the onset of myocardial infarction

International Nuclear Information System (INIS)

Shimonagata, Tsuyoshi; Nishimura, Tsunehiko; Uehara, Toshiisa; Hayashida, Kohei; Sumiyoshi, Tetsuya; Nonogi, Hiroshi; Hase, Kazuo

1991-01-01

This study evaluated the relationship between the time after onset of myocardial infarction and thallium redistribution in infarcted areas in a total of 123 patients with anterior infarction who underwent exercise thallium scintiscanning. Complete or incomplete redistribution of thallium was visually evaluated for transient perfusion defect by three physicians. Ischemic and defect scores were quantitatively determined by using circumferential profile analysis. The patients were divided into three groups: 64 patients receiving thallium scintiscanning within 3 months after onset of myocardial infarction (Group A), 25 patients receiving it at 3 months to one year after that (Group B), and 34 patients receiving it one year or later (Group C). Complete and incomplete redistributions were seen in 4% and 96%, respectively, for Group A, 38% and 62% for Group B, and 53% and 47% for Group C; and the rate of incomplete redistribution was significantly higher in Group A than the other two groups. Ischemic score was 50±32 for Group A, 46±29 for Group B, and 37±19 for Group C; and defect scores for these groups were 25±16, 24±16, and 20±18, respectively. Both ischemic and defect scores tended to be lower as the time after onset of myocardial infarction was longer. Eighteen patients, comprising 7 in Group A, 4 in Group B, and 7 in Group C, were also reinjected with thallium 201 and then reimaged at rest. These scans for Group A showed a significantly lower defect scores than the conventional thallium scans. Conventional exercise thallium scintiscanning seemed to underestimate thallium redistribution when performed early after onset of myocardial infarction. (N.K.)

Electrocardiographic changes of acute lateral wall myocardial infarction: a reappraisal based on scintigraphic localization of the infarct

International Nuclear Information System (INIS)

Movahed, A.; Becker, L.C.

1984-01-01

To determine how often acute lateral myocardial infarcts may be electrocardiographically silent, a new approach was utilized in which subjects were selected by admission thallium scintigraphy. Thirty-one patients with their first infarction were identified with moderate to severe perfusion defects of the lateral and posterolateral walls, persistent over 7 days and associated with severe wall motion abnormalities. Patients with involvement of the anterior, septal or inferior regions were not included. In nine patients, the perfusion defect extended to the anterolateral wall: all developed ST elevation and Q waves in at least one of the lateral leads (I, aVL or V6) but none showed changes in the inferior leads (II, III or aVF). In the other 22 patients, the perfusion defect was limited to the lateral and posterolateral walls: only 12 showed ST elevations (inferior leads only in 7, lateral leads only in 2, both leads in 3) and only 9 developed Q waves (inferior in all). In 8 of these 22 patients, the infarct was silent in the sense that no ST segment elevation or Q waves were seen, although ST depressions or T wave inversions, or both, in all but one patient were compatible with subendocardial infarction. The results indicate that the standard electrocardiogram is insensitive to changes in the lateral and posterolateral regions. Additional diagnostic studies are needed for proper localization and sizing of acute myocardial infarcts

Delayed ventricular septal rupture complicating acute inferior wall myocardial infarction

OpenAIRE

Cho, Jae Hyung; Sattiraju, Srinivasan; Mehta, Sanjay; Missov, Emil

2013-01-01

Background Ventricular septal rupture is a potentially fatal complication of acute myocardial infarction. Its incidence has declined with modern reperfusion therapy. In the era of percutaneous coronary interventions, it occurs a median of 18?24?hours after myocardial infarction and is most commonly associated with anterior myocardial infarction. We present a case of delayed ventricular septal rupture complicating acute inferior wall myocardial infarction. Case presentation A 53-year-old Cauca...

Scan analysis in myocardial infarction

Energy Technology Data Exchange (ETDEWEB)

Ell, P J [Landesunfallkrankenhaus, Feldkirch (Austria). Inst. fuer Strahlenmedizin

1976-08-01

Myocardial scans with sup(99m)Tc-labelled phosphates are reported to be useful in the diagnosis of acute myocardial infarction. A retrospective survey of 205 patients referred for sup(99m)Tc-phophate bone scanning and with no evidence of recent heart disease revealed an occurrence of 10% of false positive images, that is to say, uptake of phosphate in non-infarcted mayocardium. These striking findings stress the need for critical assessment of the usefulness of this diagnostic technique.

Anhedonic depression, history of depression, and anxiety as gender-specific risk factors of myocardial infarction in healthy men and women: The HUNT study

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Eva Langvik

2014-11-01

Full Text Available This prospective study examines gender-specific psychological risk factors of myocardial infarction. Out of 41,248 participants free of coronary heart disease at baseline, 822 cases of myocardial infarction were identified in the Nord-Trøndelag Health Study or the mortality register. The participants completed the Hospital Anxiety and Depression Scale. Cholesterol, blood pressure, and waist–hip ratio were measured by medical staff. Smoking, diabetes, non-fatal myocardial infarction, and history of depressive episode were self-reported. Anhedonic depression (Hospital Anxiety and Depression Scale-D ≥8 was a significant predictor of myocardial infarction in women but not in men. Gender difference in risk estimate based on Hospital Anxiety and Depression Scale-D was significant ( p  < .01. History of depressive episode was a significant predictor of myocardial infarction in men. Symptoms of anxiety (Hospital Anxiety and Depression Scale-A ≥8 reduced the risk of having a myocardial infarction.

Efficacy of Novel Carbon Nanoparticle Antioxidant Therapy in a Severe Model of Reversible Middle Cerebral Artery Stroke in Acutely Hyperglycemic Rats

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Roderic H. Fabian

2018-04-01

Full Text Available IntroductionWhile oxidative stress can be measured during transient cerebral ischemia, antioxidant therapies for ischemic stroke have been clinically unsuccessful. Many antioxidants are limited in their range and/or capacity for quenching radicals and can generate toxic intermediates overwhelming depleted endogenous protection. We developed a new antioxidant class, 40 nm × 2 nm carbon nanoparticles, hydrophilic carbon clusters, conjugated to poly(ethylene glycol termed PEG-HCCs. These particles are high-capacity superoxide dismutase mimics, are effective against hydroxyl radical, and restore the balance between nitric oxide and superoxide in the vasculature. Here, we report the effects of PEG-HCCs administered during reperfusion after transient middle cerebral artery occlusion (tMCAO by suture in the rat under hyperglycemic conditions. Hyperglycemia occurs in one-third of stroke patients and worsens clinical outcome. In animal models, this worsening occurs largely by accelerating elaboration of reactive oxygen species (ROS during reperfusion.MethodsPEG-HCCs were studied for their protective ability against hydrogen peroxide in b.End3 brain endothelial cell line and E17 primary cortical neuron cultures. In vivo, hyperglycemia was induced by streptozotocin injection 2 days before tMCAO. 58 Male Sprague-Dawley rats were analyzed. They were injected IV with PBS or PEG-HCCs (4 mg/kg 2× at the time of recanalization after either 90- or 120-min occlusion. Rats were survived for up to 3 days, and infarct volume characteristics and neurological functional outcome (modified Bederson Score were assessed.ResultsPEG-HCCs were protective against hydrogen peroxide in both culture models. In vivo improvement was found after PEG-HCCs with 90-min ischemia with reduction in infarct size (42%, hemisphere swelling (46%, hemorrhage score (53%, and improvement in Bederson score (70% (p = 0.068–0.001. Early high mortality in the 2-h in the PBS

Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both

DEFF Research Database (Denmark)

Solomon, Scott D; Zelenkofske, Steve; McMurray, John J V

2005-01-01

BACKGROUND: The risk of sudden death from cardiac causes is increased among survivors of acute myocardial infarction with reduced left ventricular systolic function. We assessed the risk and time course of sudden death in high-risk patients after myocardial infarction. METHODS: We studied 14......,609 patients with left ventricular dysfunction, heart failure, or both after myocardial infarction to assess the incidence and timing of sudden unexpected death or cardiac arrest with resuscitation in relation to the left ventricular ejection fraction. RESULTS: Of 14,609 patients, 1067 (7 percent) had an event...... percent confidence interval, 0.11 to 0.18 percent) after 2 years. Patients with a left ventricular ejection fraction of 30 percent or less were at highest risk in this early period (rate, 2.3 percent per month; 95 percent confidence interval, 1.8 to 2.8 percent). Nineteen percent of all sudden deaths...

Influence of pre-infarction angina, collateral flow, and pre-procedural TIMI flow on myocardial salvage index by cardiac magnetic resonance in patients with ST-segment elevation myocardial infarction.

Science.gov (United States)

Lønborg, Jacob; Kelbæk, Henning; Vejlstrup, Niels; Bøtker, Hans Erik; Kim, Won Yong; Holmvang, Lene; Jørgensen, Erik; Helqvist, Steffen; Saunamäki, Kari; Thuesen, Leif; Krusell, Lars Romer; Clemmensen, Peter; Engstrøm, Thomas

2012-05-01

In patients with ST-segment elevation myocardial infarction (STEMI) pre-infarction angina, pre-procedural TIMI flow and collateral flow to the myocardium supplied by the infarct related artery are suggested to be cardioprotective. We evaluated the effect of these factors on myocardial salvage index (MSI) and infarct size adjusting for area at risk in patients with STEMI treated with primary percutaneous coronary intervention. Cardiac magnetic resonance (CMR) was used to measure myocardial area at risk within 1-7 days and final infarct size 90 ± 21 days after the STEMI in 200 patients. MSI was calculated as (area-at-risk infarct size) / area-at-risk. Patients with pre-infarction angina had a median MSI of 0.80 (IQR 0.67 to 0.86) versus 0.72 (0.61 to 0.80) in those without pre-infarction angina, P = 0.004). In a regression analysis of the infarct size plotted against the area-at-risk there was a strong trend that the line for the pre-infarction angina group was below the one for the non-angina group (P = 0.05). Patients with pre-procedural TIMI flow 0/1, 2 and 3 had a median MSI of (0.69 (IQR 0.59 to 0.76), 0.78 (0.68 to 0.86) and 0.85 (0.77 to 0.91), respectively (PCollateral flow did not change MSI (P = 0.45) nor area-at-risk (P = 0.40) and no significant difference in infarct size adjusted for area at risk (P = 0.25) was observed. Pre-infarction angina increases MSI in patients with STEMI supporting the theory that pre-infarction angina leads to ischemic preconditioning. As opposed to the presence of angiographically visible collateral flow to the infarct area pre-procedural TIMI flow is strongly associated with MSI.

Role of Training and Detraining on Inflammatory and Metabolic Profile in Infarcted Rats: Influences of Cardiovascular Autonomic Nervous System

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Santana, Aline Alves; Santamarina, Aline Boveto; Oyama, Lila Missae; Caperuto, Érico Chagas; de Souza, Cláudio Teodoro; Barboza, Catarina de Andrade; Rocha, Leandro Yanase; Figueroa, Diego; Mostarda, Cristiano; Irigoyen, Maria Cláudia; Lira, Fábio Santos

2014-01-01

The aim of this study was to evaluate the effects of exercise training (ET, 50–70% of VO2 max, 5 days/week) and detraining (DT) on inflammatory and metabolic profile after myocardial infarction (MI) in rats. Male Wistar rats were divided into control (C, n = 8), sedentary infarcted (SI, n = 9), trained infarcted (TI, n = 10; 3 months of ET), and detrained infarcted (DI, n = 11; 2 months of ET + 1 month of DT). After ET and DT protocols, ventricular function and inflammation, cardiovascular autonomic modulation (spectral analysis), and adipose tissue inflammation and lipolytic pathway were evaluated. ET after MI improved cardiac and vascular autonomic modulation, and these benefits were correlated with reduced inflammatory cytokines on the heart and adipose tissue. These positive changes were sustained even after 1 month of detraining. No expressive changes were observed in oxidative stress and lipolytic pathway in experimental groups. In conclusion, our results strongly suggest that the autonomic improvement promoted by ET, and maintained even after the detraining period, was associated with reduced inflammatory profile in the left ventricle and adipose tissue of rats subjected to MI. These data encourage enhancing cardiovascular autonomic function as a therapeutic strategy for the treatment of inflammatory process triggered by MI. PMID:25045207

Role of Training and Detraining on Inflammatory and Metabolic Profile in Infarcted Rats: Influences of Cardiovascular Autonomic Nervous System

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Bruno Rodrigues

2014-01-01

Full Text Available The aim of this study was to evaluate the effects of exercise training (ET, 50–70% of VO2 max, 5 days/week and detraining (DT on inflammatory and metabolic profile after myocardial infarction (MI in rats. Male Wistar rats were divided into control (C, n=8, sedentary infarcted (SI, n=9, trained infarcted (TI,  n=10; 3 months of ET, and detrained infarcted (DI, n=11; 2 months of ET + 1 month of DT. After ET and DT protocols, ventricular function and inflammation, cardiovascular autonomic modulation (spectral analysis, and adipose tissue inflammation and lipolytic pathway were evaluated. ET after MI improved cardiac and vascular autonomic modulation, and these benefits were correlated with reduced inflammatory cytokines on the heart and adipose tissue. These positive changes were sustained even after 1 month of detraining. No expressive changes were observed in oxidative stress and lipolytic pathway in experimental groups. In conclusion, our results strongly suggest that the autonomic improvement promoted by ET, and maintained even after the detraining period, was associated with reduced inflammatory profile in the left ventricle and adipose tissue of rats subjected to MI. These data encourage enhancing cardiovascular autonomic function as a therapeutic strategy for the treatment of inflammatory process triggered by MI.

Cardioprotective Effect of the Compound Yangshen Granule in Rat Models with Acute Myocardial Infarction

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Xie Ming

2012-01-01

Full Text Available The protective effect of Compound Yangshen Granules was observed in myocardial infarction rat model. Rats were randomly divided into 6 groups: the model group, the control group (sham operated, the positive drug group, and small, medium, and large dosage of the Yangshen granule groups, respectively. The rats in the 3 Yangshen granule groups were orally administrated with 0.7 g/kg, 1.4 g/kg, and 2.8 g/kg for 7 consecutive days, whereas the rats of the positive drug group treated with 0.14 g/kg of Danshen Dropping Pills, and rats in the control and model groups orally administrated with saline. The rat model of acute myocardial infarction was established with ligation of coronary artery. Electrocardiograms at different time points, the blood rheology, myocardial enzymes, infarct size, and myocardial morphologic changes were measured. The results demonstrated that the granules could improve blood rheology, decrease st-segment of electrocardiograms and the activities of LDH and CK in serum, reduce myocardial infarction size, and alleviate myocardial histopathologic changes. In addition, the effect of the granules depended on the dose administrated orally. The results suggest that the Yangshen granules could produce cardioprotection effect and have potential benefits in the prevention of ischemic heart disease.

TIA model is attainable in Wistar rats by intraluminal occlusion of the MCA for 10min or shorter.

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Durukan Tolvanen, A; Tatlisumak, E; Pedrono, E; Abo-Ramadan, U; Tatlisumak, T

2017-05-15

Transient ischemic attack (TIA) has received only little attention in the experimental research field. Recently, we introduced a TIA model for mice, and here we set similar principles for simulating this human condition in Wistar rats. In the model: 1) transient nature of the event is ensured, and 2) 24h after the event animals are free from any sensorimotor deficit and from any detectable lesion by magnetic resonance imaging (MRI). Animals experienced varying durations of ischemia (5, 10, 12.5, 15, 25, and 30min, n=6-8pergroup) by intraluminal middle cerebral artery occlusion (MCAO). Ischemia severity and reperfusion rates were controlled by cerebral blood flow measurements. Sensorimotor neurological evaluations and MRI at 24h differentiated between TIA and ischemic stroke. Hematoxylin and eosin staining and apoptotic cell counts revealed pathological correlates of the event. We found that already 12.5min of ischemia was long enough to induce ischemic stroke in Wistar rats. Ten min or shorter durations induced neither gross neurological deficits nor infarcts visible on MRI, but histologically caused selective neuronal necrosis. A separate group of animals with 10min of ischemia followed up to 1week after reperfusion remained free of infarction and any MRI signal change. Thus, 10min or shorter focal cerebral ischemia induced by intraluminal MCAO in Wistar rats provides a clinically relevant TIA the rat. This model is useful for studying molecular correlates of TIA. Copyright © 2017 Elsevier B.V. All rights reserved.

Comparsion between Intravenous Delivered Human Fetal Bone Marrow Mesenchymal Stromal Cells and Mononuclear Cells in the Treatment of Rat Cerebral Infarct.

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Huang, Ai-Hua; Zhang, Ping-Ping; Zhang, Bin; Ma, Bu-Qing; Guan, Yun-Qian; Zhou, Yi-Dan

2016-10-10

Objective To compare the effecacy of human mesenchymal stromal cell (hMSC) with human mononuclear cell (hMNC) in treating rat cerebral infarct.Methods The SD rat models of cerebral infarct were established by distal middle cerebral artery occlusion (dMCAO). Rats were divided into four groups: sham,ischemia vehicle,MSC,and MNC transplantation groups. For the transplantation group,1×10 6 hMSCs or hMNCs were intravascularly transplanted into the tail vein 1 hour after the ischemia onset. The ischemia vehicle group received dMCAO surgery and intravascular saline injection 1,3,5,and 7 days after the ischemia onset,and then behavioral tests were performed. At 48 h after the ischemia onset,the abundance of Iba- 1,the symbol of activated microglia,was evaluated in the peri-ischemia striatum area; meanwhile,the neurotrophic factors such as glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) in ipsilateral peri-ischemia striatum area were also measured. Results The relative infarct volume in ischemia vehicle group,hMSC group,and hMNC transplantation group were (37.85±4.40)%,(33.41±3.82)%,and (30.23±3.63)%,respectively. The infarct volumes of MSC group (t=2.100,P=0.034) and MNC group (t=2.109,P=0.0009) were significantly smaller than that of ischemia vehicle group,and that of MNC group was significantly smaller than that of MSC group (t=1.743,P=0.043). One day after transplantation,the score of ischemia vehicle group in limb placing test was (4.32±0.71)%,which was significantly lower than that in sham group (9.73±0.36)% (t=2.178,P=8.61×10 -11 ). The scores of MSC and MNC group,which were (5.09±0.62)% (t=2.1009,P=0.024) and (5.90±0.68)% (t=2.1008,P=0.0001),respectively,were significantly higher than that of ischemia vehicle group; also,the score of MNC group was significantly higher than that of MSC group(t=2.1009,P=0.0165). The contralateral forelimb scores of MSC and MNC groups in beam walking test were (5.56±0.86)% (t=2

Hepatic infarction in HELLP syndrome; a case report

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Kim, Mi Jeong; Kim, Hong [Keimyung Univ. School of Medicine, Taegu (Korea, Republic of)

2000-11-01

Hepatic infarction is a rare but potentially life-threatening complication of pregnancy-associated preeclampsia or HELLP (hemolysis, elevated liver function tests, low platelets) syndrome. We present a case of hepatic infarction subsequent to HELLP syndrome and occurring during the immediate postpartum, and the associated radiologic findings. Sonography revealed poorly defined hypoechoic zones of infarction. Computed tomography(CT) demonstrated the characteristic features of nonenhancing, low attenuation, relatively well-defined, wedge shaped or geographic hepatic lesions, without mass effect.

Hepatic infarction in HELLP syndrome; a case report

International Nuclear Information System (INIS)

Kim, Mi Jeong; Kim, Hong

2000-01-01

Hepatic infarction is a rare but potentially life-threatening complication of pregnancy-associated preeclampsia or HELLP (hemolysis, elevated liver function tests, low platelets) syndrome. We present a case of hepatic infarction subsequent to HELLP syndrome and occurring during the immediate postpartum, and the associated radiologic findings. Sonography revealed poorly defined hypoechoic zones of infarction. Computed tomography(CT) demonstrated the characteristic features of nonenhancing, low attenuation, relatively well-defined, wedge shaped or geographic hepatic lesions, without mass effect

Segmentation of Hyperacute Cerebral Infarcts Based on Sparse Representation of Diffusion Weighted Imaging

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Xiaodong Zhang

2016-01-01

Full Text Available Segmentation of infarcts at hyperacute stage is challenging as they exhibit substantial variability which may even be hard for experts to delineate manually. In this paper, a sparse representation based classification method is explored. For each patient, four volumetric data items including three volumes of diffusion weighted imaging and a computed asymmetry map are employed to extract patch features which are then fed to dictionary learning and classification based on sparse representation. Elastic net is adopted to replace the traditional L0-norm/L1-norm constraints on sparse representation to stabilize sparse code. To decrease computation cost and to reduce false positives, regions-of-interest are determined to confine candidate infarct voxels. The proposed method has been validated on 98 consecutive patients recruited within 6 hours from onset. It is shown that the proposed method could handle well infarcts with intensity variability and ill-defined edges to yield significantly higher Dice coefficient (0.755 ± 0.118 than the other two methods and their enhanced versions by confining their segmentations within the regions-of-interest (average Dice coefficient less than 0.610. The proposed method could provide a potential tool to quantify infarcts from diffusion weighted imaging at hyperacute stage with accuracy and speed to assist the decision making especially for thrombolytic therapy.

The effect of progressive muscle relaxation techniques on anxiety in Patients with myocardial infarction

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Mozhgan Jariani

2011-12-01

Conclusion: progressive muscle relaxation can reduce the amount of anxiety, and systolic and diastolic blood pressure of the patients with myocardial infarction hospitalized in CCU ward, therefore it can play an effective role as a supplement non-medicinal, simple and cheap treatment for these patients

Calcification within the lesion of an old cerebral infarction

International Nuclear Information System (INIS)

Hanyu, Haruo; Hagiwara, Akiyoshi; Yamaguchi, Katsuhiko; Imamura, Toshiharu; Iwamoto, Toshihiko; Katsunuma, Hideyo

1987-01-01

We described a 68-year-old woman with marked calcification in the lesion of an old cerebral infarction. Calcified deposits in an old infarcted area of the left middle cerebral artery were demonstrated by CT 9 months after she had suffered a stroke, probably because of an embolism. There have been few reports of calcification associated with cerebral infarction. (author)

DEPRESSION, ANXIETY AND MYOCARDIAL INFARCTION: EVERYTHING JUST BEGINS (PART I

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Y. A. Vasyuk

2015-12-01

Full Text Available A review is devoted to a comorbidity of myocardial infarction and anxious and depressive disorders. In the first part data concerning prevalence of depression in myocardial infarction, pathophysiological mechanisms connecting depression and ischemic heart disease (IHD are given. Influence of concomitant depressive disorders on clinical state and forecast of patients after myocardial infarction is discussed. The second part of the review (Rational Pharmacother. Cardiol. 2007, 4 will be devoted to the anxious disorders in myocardial infarction as well as to influence of anxious and depressive disorders on life quality of patients with myocardial infarction. Besides, contemporary approaches to the therapy of anxious and depressive disorders in patients with IHD will be discussed.

DEPRESSION, ANXIETY AND MYOCARDIAL INFARCTION: EVERYTHING JUST BEGINS. PART II

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Y. A. Vasyuk

2015-12-01

Full Text Available A review is devoted to a comorbidity of myocardial infarction and anxious and depressive disorders. In the first part (Rational Pharmacother. Cardiol. 2007;3:41-51 data concerning prevalence of depression in myocardial infarction, pathophysiological mechanisms connecting depression and ischemic heart disease (IHD were given. Influence of concomitant depressive disorders on clinical state and forecast of patients after myocardial infarction was discussed. The second part of the review is devoted to the anxious disorders in myocardial infarction as well as to influence of anxious and depressive disorders on life quality of patients with myocardial infarction. Besides, contemporary approaches to the therapy of anxious and depressive disorders in patients with IHD are discussed.

Time course of infarct healing and left ventricular remodelling in patients with reperfused ST segment elevation myocardial infarction using comprehensive magnetic resonance imaging

International Nuclear Information System (INIS)

Ganame, Javier; Messalli, Giancarlo; Dymarkowski, Steven; Abbasi, Kayvan; Bogaert, Jan; Masci, Pier Giorgio; Werf, Frans van de; Janssens, Stefan

2011-01-01

To describe the time course of myocardial infarct (MI) healing and left ventricular (LV) remodelling and to assess factors predicting LV remodelling using cardiac MRI. In 58 successfully reperfused MI patients, MRI was performed at baseline, 4 months (4M), and 1 year (1Y) post MI Infarct size decreased between baseline and 4M (p < 0.001), but not at 1Y; i.e. 18 ± 11%, 12 ± 8%, 11 ± 6% of LV mass respectively; this was associated with LV mass reduction. Infarct and adjacent wall thinning was found at 4M, whereas significant remote wall thinning was measured at 1Y. LV end-diastolic and end-systolic volumes significantly increased at 1Y, p < 0.05 at 1Y vs. baseline and vs. 4M; this was associated with increased LV sphericity index. No regional or global LV functional improvement was found at follow-up. Baseline infarct size was the strongest predictor of adverse LV remodelling. Infarct healing, with shrinkage of infarcted myocardium and wall thinning, occurs early post-MI as reflected by loss in LV mass and adjacent myocardial remodelling. Longer follow-up demonstrates ongoing remote myocardial and ventricular remodelling. Infarct size at baseline predicts long-term LV remodelling and represents an important parameter for tailoring future post-MI pharmacological therapies designed to prevent heart failure. (orig.)

Challenges in secondary prevention after acute myocardial infarction

DEFF Research Database (Denmark)

Piepoli, Massimo F; Corrà, Ugo; Dendale, Paul

2017-01-01

in the first year and approximately 50% of major coronary events occur in those with a previous hospital discharge diagnosis of ischaemic heart disease. The people behind these numbers spur this call for action. Prevention after myocardial infarction is crucial to reduce risk and suffering. Evidence...... document in which the existing gaps for secondary prevention strategies are reviewed. Effective interventions in relation to the patients, healthcare providers and healthcare systems are proposed and discussed. Finally, innovative strategies in hospital as well as in outpatient and long-term settings...

An evaluation of MR diffusion imaging in the diagnosis of cerebral infarction

International Nuclear Information System (INIS)

Xiong Weijian; Feng Shaolan; Zhou Zhijuan; Lin Yan

2005-01-01

Objective: To evaluate MR diffusion-weighted imaging (DWI) in the diagnosis of cerebral infarction. Methods: Thirty patients with clinically-diagnosed acute (6 hyper-acute and 24 acute) cerebral infarction scanned with both conventional and DW MRI. Results: DWI had the 100% sensitivity for hyper-acute and acute cerebral infarction. Hyper-acute and acute cerebral infarctions all showed hyper intensity on DWI. All 6 hyper-acute cerebral infarctions were only revealed on DWI but silent on conventional MRI. Conclusion: DWI is a useful MR technique, which is superior to conventional MR sequences in revealing the hyper-acute, acute cerebral infarct. DWI has a higher sensitivity for acute, especially hyper-acute cerebral infarction than conventional MRI. (authors)

Using a Cloud Computing System to Reduce Door-to-Balloon Time in Acute ST-Elevation Myocardial Infarction Patients Transferred for Percutaneous Coronary Intervention

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Chi-Kung Ho

2017-01-01

Full Text Available Background. This study evaluated the impact on clinical outcomes using a cloud computing system to reduce percutaneous coronary intervention hospital door-to-balloon (DTB time for ST segment elevation myocardial infarction (STEMI. Methods. A total of 369 patients before and after implementation of the transfer protocol were enrolled. Of these patients, 262 were transferred through protocol while the other 107 patients were transferred through the traditional referral process. Results. There were no significant differences in DTB time, pain to door of STEMI receiving center arrival time, and pain to balloon time between the two groups. Pain to electrocardiography time in patients with Killip I/II and catheterization laboratory to balloon time in patients with Killip III/IV were significantly reduced in transferred through protocol group compared to in traditional referral process group (both p<0.05. There were also no remarkable differences in the complication rate and 30-day mortality between two groups. The multivariate analysis revealed that the independent predictors of 30-day mortality were elderly patients, advanced Killip score, and higher level of troponin-I. Conclusions. This study showed that patients transferred through our present protocol could reduce pain to electrocardiography and catheterization laboratory to balloon time in Killip I/II and III/IV patients separately. However, this study showed that using a cloud computing system in our present protocol did not reduce DTB time.

U0126 attenuates cerebral vasoconstriction and improves long-term neurologic outcome after stroke in female rats

DEFF Research Database (Denmark)

Ahnstedt, Hilda; Mostajeran, Maryam; Blixt, Frank W

2015-01-01

, responses to this treatment in females and long-term effects on outcome are not known. Initial experiments used in vitro organ culture of cerebral arteries, confirming ERK1/2 activation and increased ETB receptor-mediated vasoconstriction in female cerebral arteries. Transient middle cerebral artery......-mediated contraction was studied with myograph and protein expression with immunohistochemistry. In vitro organ culture and tMCAO resulted in vascular ETB receptor upregulation and activation of ERK1/2 that was prevented by U0126. Although no effect on infarct size, U0126 improved the long-term neurologic function...

Pathogenesis and prognosis of bilateral thalamic infarction

International Nuclear Information System (INIS)

Nakase, Taizen; Ogura, Naoko; Maeda, Tetsuya; Yamazaki, Takashi; Kameda, Tomoaki; Sato, Yuichi; Nagata, Ken

2008-01-01

Only a few reports have discussed the detailed clinical symptoms and pathogenesis of bilateral thalamic infarction. The thalamus is composed of different functional nuclei and supplied by vessels containing several variations from the main arteries, leading to difficulty in the precise evaluation of bilateral thalamic infarction. In the present study, we assessed the prognosis of bilateral thalamic infarction based on the distribution of stroke lesions. From among the consecutive ischemic stroke patients admitted to hospital between April 2001 and March 2005, cases of acute bilateral thalamic infarction were selected for this study (n=9; 65.1±13.6 y.o.). The stroke lesions and vascular abnormalities were investigated by magnetic resonance imaging and magnetic resonance angiography on admission. Outcome was evaluated from the modified Rankin scale (mRS) at discharge. Good outcome patients (mRS 0-2; n=5) showed memory disturbance, cognitive impairment and hypersomnia. On the other hand, quadriplegia, oculomotor disturbance and bulbar palsy were observed in the poor outcome patients (mRS≥4; n=4). The critical features of a poor outcome were the age at onset (72.0±15.3 vs. 58.2±11.9 y.o.), inclusion of brainstem lesions and total occlusion of the basilar artery. In conclusion, older age at onset and/or basilar artery occlusion may be critical factors for predicting a poor outcome in bilateral thalamic infarction cases. (author)

Brain stem infarction: Imaging diagnosis and endovascular therapy

International Nuclear Information System (INIS)

Schulte-Altedorneburg, G.; Mayer, T.E.

2004-01-01

This review article describes the vascular anatomy and pathophysiology of the vertebrobasilar ischaemia as well as the most important clinical syndromes of brainstem infarctions. An overview of the literature presents the role of invasive and non-invasive techniques (ultrasound, MRI, MRA, CT, CTA, intraarterial angiography) to diagnose an acute brainstem infarction. Current concepts are described for treating acute vertebrobasilar thrombosis, including local intraarterial fibrinolysis, mechanical recanalization and medical treatment, and for preventing brainstem infarction, including angioplasty and stent-assisted angioplasty of the brainstem supplying arteries. (orig.)

Malrotation with midgut volvulus: CT findings of bowel infarction

International Nuclear Information System (INIS)

Aidlen, Jeremy; Anupindi, Sudha A.; Jaramillo, Diego; Doody, Daniel P.

2005-01-01

Midgut volvulus, the most common serious complication of malrotation, can be diagnosed using conventional contrast fluoroscopy, US or CT. CT is a quick and comprehensive examination in the evaluation of complex acute abdominal pathology in children. Contrast-enhanced CT can readily help the radiologist recognize perfusion abnormalities of the bowel, which is vital for reducing morbidity and mortality in affected children. Our case emphasizes and demonstrates additional CT features of bowel infarction in a child with a proven malrotation with midgut volvulus. (orig.)

Malrotation with midgut volvulus: CT findings of bowel infarction

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Aidlen, Jeremy [University of Massachusetts Medical Center, Department of Surgery, Worchester (United States); Anupindi, Sudha A.; Jaramillo, Diego [Massachusetts General Hospital, Pediatric Radiology, Boston, MA (United States); Doody, Daniel P. [Massachusetts General Hospital, Department of Pediatric Surgery, Boston, MA (United States)

2005-05-01

Midgut volvulus, the most common serious complication of malrotation, can be diagnosed using conventional contrast fluoroscopy, US or CT. CT is a quick and comprehensive examination in the evaluation of complex acute abdominal pathology in children. Contrast-enhanced CT can readily help the radiologist recognize perfusion abnormalities of the bowel, which is vital for reducing morbidity and mortality in affected children. Our case emphasizes and demonstrates additional CT features of bowel infarction in a child with a proven malrotation with midgut volvulus. (orig.)

A randomized, double-blinded, placebo-controlled multicenter trial of adenosine as an adjunct to reperfusion in the treatment of acute myocardial infarction (AMISTAD-II).

Science.gov (United States)

Ross, Allan M; Gibbons, Raymond J; Stone, Gregg W; Kloner, Robert A; Alexander, R Wayne

2005-06-07

The purpose of this research was to determine the effect of intravenous adenosine on clinical outcomes and infarct size in ST-segment elevation myocardial infarction (STEMI) patients undergoing reperfusion therapy. Previous small studies suggest that adenosine may reduce the size of an evolving infarction. Patients (n = 2,118) with evolving anterior STEMI receiving thrombolysis or primary angioplasty were randomized to a 3-h infusion of either adenosine 50 or 70 microg/kg/min or of placebo. The primary end point was new congestive heart failure (CHF) beginning >24 h after randomization, or the first re-hospitalization for CHF, or death from any cause within six months. Infarct size was measured in a subset of 243 patients by technetium-99m sestamibi tomography. There was no difference in the primary end point between placebo (17.9%) and either the pooled adenosine dose groups (16.3%) or, separately, the 50-microg/kg/min dose and 70-microg/kg/min groups (16.5% vs. 16.1%, respectively, p = 0.43). The pooled adenosine group trended toward a smaller median infarct size compared with the placebo group, 17% versus 27% (p = 0.074). A dose-response relationship with final median infarct size was seen: 11% at the high dose (p = 0.023 vs. placebo) and 23% at the low dose (p = NS vs. placebo). Infarct size and occurrence of a primary end point were significantly related (p < 0.001). Clinical outcomes in patients with STEMI undergoing reperfusion therapy were not significantly improved with adenosine, although infarct size was reduced with the 70-microg/kg/min adenosine infusion, a finding that correlated with fewer adverse clinical events. A larger study limited to the 70-microg/kg/min dose is, therefore, warranted.

Electro-mechanical characteristics of myocardial infarction border zones and ventricular arrhythmic risk: novel insights from grid-tagged cardiac magnetic resonance imaging

International Nuclear Information System (INIS)

Wong, Dennis T.L.; Weightman, Michael J.; Baumert, Mathias; Tayeb, Hussam; Richardson, James D.; Puri, Rishi; Bertaso, Angela G.; Roberts-Thomson, Kurt C.; Sanders, Prashanthan; Worthley, Matthew I.; Worthley, Stephen G.

2012-01-01

To investigate whether grid-tag myocardial strain evaluation can characterise 'border-zone' peri-infarct region and identify patients at risk of ventricular arrhythmia as the peri-infarct myocardial zone may represent an important contributor to ventricular arrhythmia following ST-segment elevation myocardial infarction (STEMI). Forty-five patients with STEMI underwent cardiac magnetic resonance (CMR) imaging on days 3 and 90 following primary percutaneous coronary intervention (PCI). Circumferential peak circumferential systolic strain (CS) and strain rate (CSR) were calculated from grid-tagged images. Myocardial segments were classified into 'infarct', 'border-zone', 'adjacent' and 'remote' regions by late-gadolinium enhancement distribution. The relationship between CS and CSR and these distinct myocardial regions was assessed. Ambulatory Holter monitoring was performed 14 days post myocardial infarction (MI) to estimate ventricular arrhythmia risk via evaluation of heart-rate variability (HRV). We analysed 1,222 myocardial segments. Remote and adjacent regions had near-normal parameters of CS and CSR. Border-zone regions had intermediate CS (-9.0 ± 4.6 vs -5.9 ± 7.4, P < 0.001) and CSR (-86.4 ± 33.3 vs -73.5 ± 51.4, P < 0.001) severity compared with infarct regions. Patients with 'border-zone' peri-infarct regions had reduced very-low-frequency power on HRV analysis, which is a surrogate for ventricular arrhythmia risk (P = 0.03). Grid-tagged CMR-derived myocardial strain accurately characterises the mechanical characteristics of 'border-zone' peri-infarct region. Presence of 'border-zone' peri-infarct region correlated with a surrogate marker of heightened arrhythmia risk following STEMI. (orig.)

Electrocardiographic infarct size assessment after thrombolysis: insights from the Acute Myocardial Infarction STudy ADenosine (AMISTAD) trial.

Science.gov (United States)

Barbagelata, Alejandro; Di Carli, Marcelo F; Califf, Robert M; Garg, Jyotsna; Birnbaum, Yochai; Grinfeld, Liliana; Gibbons, Raymond J; Granger, Christopher B; Goodman, Shaun G; Wagner, Galen S; Mahaffey, Kenneth W

2005-10-01

Noninvasive methods are needed to evaluate reperfusion success in patients with acute myocardial infarction (MI). The AMISTAD trial was analyzed to compare MI size and myocardial salvage determined by electrocardiogram (ECG) with technetium Tc 99m sestamibi single-photon emission computerized tomography (SPECT) imaging. Of 236 patients enrolled in AMISTAD, 166 (70 %) with no ECG confounding factors and no prior MI were included in this analysis. Of these, group 1 (126 patients, 53%) had final infarct size (FIS) available by both ECG and SPECT. Group 2 (56 patients, 24%) had myocardium at risk, FIS, and salvage index (SI) assessed by both SPECT and ECG techniques. Aldrich/Clemmensen scores for myocardium at risk and the Selvester QRS score for final MI size were used. Salvage index was calculated as follows: SI = (myocardium at risk-FIS)/(myocardium at risk). In group 1, FIS was 15% (6, 24) as measured by ECG and 11% (2, 27) as measured by SPECT. In the adenosine group, FIS was 12% (6, 21) and 11% (2, 22). In the placebo group, FIS was 16.5% (7.5, 24) and 11.5% (3.0, 38.5) by ECG and SPECT, respectively. The overall correlation between SPECT and ECG for FIS was 0.58 (P = .0001): 0.60 in the placebo group (P = .0001) and 0.54 (P = .0001) in the adenosine group. In group 2, myocardium at risk was 23% (17, 30) and 26% (10, 50) with ECG and SPECT, respectively (P = .0066). Final infarct size was 17% (6, 21) and 12% (1, 24) (P < .0001). The SI was 29% (-7, 57) and 46% (15, 79) with ECG and SPECT, respectively (P = .0510). The ECG measurement of infarct size has a moderate relationship with SPECT infarct size measurements in the population with available assessments. This ECG algorithm must further be validated on clinical outcomes.

Measurement of the infarcted area by 201Tl myocardial emission CT

International Nuclear Information System (INIS)

Tamaki, Shunichi; Murakami, Tomoyuki; Kambara, Hirofumi

1982-01-01

201 Tl-ECT was performed in 28 cases 4 weeks after the onset of acute myocardial infarction to calculate the volume of infarction for comparison with the CK-MB infarction size obtained in the acute phase. The infarct area obtained by two-dimensional 201 Tl scintigraphy in 18 cases treated by the conventional method showed a positive correlation with the CK-MB infarct size, but the volume of infarction by 201 Tl-ECT produced a better correlation. In the group with successful thrombolysis, the serum CK-MB level reached a peak soon after the onset, accompanied by release of more CK-MB for a constant volume of infarction obtained by 201 Tl-ECT, as compared with the group with unsuccessful thrombolysis or conventional therapy. This suggests the involvement of washout phenomenon by reperfusion. Although there are some limitations, the three-dimensional detection of the distribution of myocardial blood flow by 201 Tl-ECT is useful, covering disadvantages of two-dimensional images. (Chiba, N.)

Examining the subcortical infarcts in the era of acute multimodality CT imaging

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Mindy Tan

2016-12-01

Full Text Available Background: Lacunar infarcts have been characterized as small subcortical infarcts, resulting from in situ microatheroma or lipohyalinosis in small vessels. Based on this hypothesis, such infarcts should not be associated with large areas of perfusion deficits extending beyond subcortical regions to involve cortical regions. By contrast, selected small subcortical infarcts, as defined by MR imaging in the subacute or chronic stage, may initially have large perfusion deficits or related large vessel occlusions. These infarcts with ‘lacunar’ phenotype may also be caused by disease in the parent vessel and may have very different stroke mechanisms from small vessel disease. Our aim was to describe differences in imaging characteristics between patients with small subcortical infarction with ‘lacunar phenotype’ from those with lacunar mechanism. Methods: Patients undergoing acute CT Perfusion/angiography (CTP/CTA within 6 hours of symptom onset and follow-up magnetic resonance imaging (MRI for ischaemic stroke were included (2009-2013. A lacunar infarct was defined as a single subcortical infarct (SSI ≤20 mm on follow-up MRI. Presence of perfusion deficits, vessel occlusion and infarct dimensions were compared between lacunar infarcts and other topographical infarct types. Results: Overall, 182 patients (mean age 66.4±15.3 years, 66% male were included. SSI occurred in 31 (17% patients. Of these, 12 (39% patients had a perfusion deficit compared with those with any cortical infarction (120/142, 67%, and the smallest SSI with a perfusion deficit had a diameter of <5mm. The majority of patients with SSI (8/12, 66.7% had a relevant vessel occlusion. A quarter of SSIs had a large-artery stroke mechanism evident on acute CTP/CTA. Lacunar mechanism was present in 3/8 patients with corona radiata, 5/10 lentiform nucleus, 5/6 posterior limb of internal capsule PLIC, 3/5 thalamic infarcts and 1/2 miscellaneous locations. There was a trend toward

Medical image of the week: artery of Percheron infarction

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Ta TT

2017-03-01

Full Text Available No abstract available. Article truncated after 150 words. A 55-year-old African-American man presented to the Emergency Department for acute altered mental status which started 4 hours ago. His medical history was significant for heart failure with reduced ejection fraction, diabetes mellitus, marijuana and opioid use. On admission, the patient appeared to be in a deep sleep, unarousable, with grimacing to noxious stimuli. He occasionally moved all extremities. He was intubated for airway protection. Initial CT head non-contrast demonstrated a previous right MCA infarct, with no new acute hemorrhage. MRI/MRA brain revealed complete infarction of the artery of Percheron (AOP, likely due to a left ventricular thrombus (Figure 1. The patient remained somnolent throughout hospitalization with minimal neurologic improvement, and was ultimately transferred to a long-term care facility after a tracheostomy and PEG placement. The artery of Percheron is a rare, normal intracranial vascular variant in which a single arterial trunk originates from the posterior cerebral artery, giving rise …

The thrombospondin-1 N700S polymorphism is associated with early myocardial infarction without altering von Willebrand factor multimer size.

Science.gov (United States)

Zwicker, Jeffrey I; Peyvandi, Flora; Palla, Roberta; Lombardi, Rossana; Canciani, Maria Teresa; Cairo, Andrea; Ardissino, Diego; Bernardinelli, Luisa; Bauer, Kenneth A; Lawler, Jack; Mannucci, Pier

2006-08-15

The N700S polymorphism of thrombospondin-1 (TSP-1) has been identified as a potential genetic risk factor for myocardial infarction (MI). In a large case-control study of 1425 individuals who survived a myocardial infarction prior to age 45, the N700S polymorphism was a significant risk factor for myocardial infarction in both homozygous (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.1-3.3, P = .01) and heterozygous carriers of the S700 allele (OR 1.4, 95% CI 1.1-3.3, P = .01). TSP-1 has been shown to reduce von Willebrand factor (VWF) multimer size, and the domain responsible for VWF-reducing activity has been localized to the calcium-binding C-terminal sequence. As the N700S polymorphism was previously shown to alter the function of this domain, we investigated whether the altered VWF-reducing activity of TSP-1 underlies the observed prothrombotic phenotype. The TSP1 N700S polymorphism did not influence VWF multimer size in patients homozygous for either allele nor was there a significant reduction of VWF multimer size following incubation with recombinant N700S fragments or platelet-derived TSP-1.

[Prognosis significance of blood homocysteine after myocardial infarction].

Science.gov (United States)

Reis, R P; Azinheira, J; Reis, H P; Bordalo e Sá, A; Tavares, J; Adão, M; Santos, A L; Pina, J E; Correia, J M; Luís, A S

2000-05-01

Homocysteinemia is an independent risk factor of coronary artery disease and of myocardial infarction. In the present study we intend to relate fasting homocystein levels to prognosis after a myocardial infarction. From 1990 to 1992, we studied fasting homocysteinemia levels on a group of 112 patients aged under 56 years that had suffered a myocardial infarction between 3 and 12 months before. We obtained, the patients names, addresses, phone numbers and physicians' name. Seven years later (on average) we collected data regarding the patients evolution, consulting medical records, their physicians or by personal contact. We evaluated complications, namely mortality, vascular morbidity, such as unstable angina, re-infarction, stroke, and the need for invasive procedures (catheterism, PTCA, CABG). According to previous studies of the group, we used a cut-point of 10.10 mumol/L to define patients with normal or pathological levels of homocysteinemia. We excluded all patients that took vitamin B supplements, co-factors of HC metabolism, during this follow-up. We were able to obtain data on 110 patients. Patients with normal HC levels (n = 62) presented less global complications (26 versus 72%, p homocystein levels (n = 48), those with higher homocystein levels presented a higher degree of complications. In this population with myocardial infarction under 56 years of age, a high homocysteinemia level is an important prognostic factor. This study suggests that we can improve the prognosis and decrease the complications after myocardial infarction by lowering elevated homocystein levels.

Stress Induced Cardiomyopathy Triggered by Acute Myocardial Infarction: A Case Series Challenging the Mayo Clinic Definition.

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Christodoulidis, Georgios; Kundoor, Vishwa; Kaluski, Edo

2017-08-28

BACKGROUND Various physical and emotional factors have been previously described as triggers for stress induced cardiomyopathy. However, acute myocardial infarction as a trigger has never been reported. CASE REPORT We describe four patients who presented with an acute myocardial infarction, in whom the initial echocardiography revealed wall motion abnormalities extending beyond the coronary distribution of the infarct artery. Of the four patients identified, the mean age was 59 years; three patients were women and two patients had underlying psychiatric history. Electrocardiogram revealed ST elevation in the anterior leads in three patients; QTc was prolonged in all cases. All patients had ≤ moderately elevated troponin. Single culprit lesion was found uniformly in the proximal or mid left anterior descending artery. Initial echocardiography revealed severely reduced ejection fraction with relative sparing of the basal segments, whereas early repeat echocardiography revealed significant improvement in the left ventricular function in all patients. CONCLUSIONS This is the first case series demonstrating that acute myocardial infarction can trigger stress induced cardiomyopathy. Extensive reversible wall motion abnormalities, beyond the ones expected from angiography, accompanied by modest elevation in troponin and marked QTc prolongation, suggest superimposed stress induced cardiomyopathy.

Pontine infarction with pure motor hemiparesis or hemiplegia: A prospective study

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Zhang Suping

2009-06-01

Full Text Available Abstract Background The study aimed to prospectively observe the clinical and neuroimaging features of pontine infarction with pure motor hemiparesis (PMH or hemiplegia at early stage. Methods In 118 consecutive selected patients with the first-ever ischemic stroke within 6 hours after onset, fifty of them presented with PMH or hemiplegia and had negative acute computed tomography (CT scans, then magnetic resonance imaging (MRI confirmed the corresponding infarcts in pons or cerebrum. The clinical and neuroimaging features of the pontine infarctions were compared with those of cerebral infarctions. Results The pontine infarction with PMH or hemiplegia accounted for 10.2% (12/118 of all first-ever ischemic stroke patients and 24% (12/50 of the patients with both PMH or hemiplegia and acute negative CT scans. Compared to the patients with cerebral infarction, the patients with pontine infarction had more frequency of diabetes mellitus (50.0% vs 5.3%, P = 0.001, nonvertiginous dizziness at onset (58.3% vs 21.1%, P = 0.036 and a progressive course (33.3% vs 2.6%, P = 0.011. Conclusion The pontine infarction may present as PMH or hemiplegia with more frequency of nonvertiginous dizziness, a progressive course and diabetes mellitus. MRI can confirm the infarct location in the basal pons at early stage after stroke onset.

Neuroprotective Effect of Curcumin Against Cerebral Ischemia-Reperfusion Via Mediating Autophagy and Inflammation.

Science.gov (United States)

Huang, Lifa; Chen, Chengwei; Zhang, Xin; Li, Xu; Chen, Zupeng; Yang, Chao; Liang, Xiaolong; Zhu, Guochong; Xu, Zhen

2018-01-01

Curcumin, a polyphenolic compound extracted from Curcuma longa, has drawn attention for its effective bioactivities against ischemia-induced injury. This study aimed to evaluate the neuroprotective effect of curcumin and investigate the underlying mechanism that mediates autophagy and inflammation in an animal model of middle cerebral artery occlusion (MCAO) in rats. Curcumin was delivered to Sprague Dawley male rats at a dose of 200 mg/kg curcumin by intraperitoneal injection 30 min after ischemia-reperfusion (I/R). LY294002, a specific inhibitor of the PI3K/Akt/mTOR pathway, as well as anisomycin, an activator of TLR4/p38/MAPK, was administered by ventricle injection 30 min before MCAO. The same volume of saline was given as a control. Brain infarction and neurological function were determined 24 h post-MCAO. Immunoblotting and immunofluorescence were used to detect alterations in autophagy-relevant proteins Akt, p-Akt, mTOR, p-mTOR, LC3-II, and LC3-I, and inflammation-related proteins TLR4, p-38, p-p38, and IL-1 in the ipsilateral hemisphere. Cerebral I/R injury resulted in significant alterations of LC3-II/LC3-I, IL-1, TLR4, and p-p38. Curcumin in MCAO rats significantly improved brain damage and neurological function by upregulating p-Akt and p-mTOR and downregulating LC3-II/LC3-I, IL-1, TLR4, p-38, and p-p38. However, these protective effects against ischemia could be suppressed when LY294002 or anisomycin was included. Curcumin exerts neuroprotective effects by attenuating autophagic activities through mediating the PI3K/Akt/mTOR pathway, while also suppressing an inflammatory reaction by regulating the TLR4/p38/MAPK pathway. Furthermore, this study indicates that curcumin could be an effective therapy for patients afflicted with ischemia.

Final infarct size measured by cardiovascular magnetic resonance in patients with ST elevation myocardial infarction predicts long-term clinical outcome

DEFF Research Database (Denmark)

Lønborg, Jacob Thomsen; Vejlstrup, Niels Grove; Kelbæk, Henning Skov

2013-01-01

AIMS: Tailored heart failure treatment and risk assessment in patients following ST-segment elevation myocardial infarction (STEMI) is mainly based on the assessment of the left ventricular (LV) ejection fraction (EF). Assessment of the final infarct size in addition to the LVEF may improve...

Do episodes of anger trigger myocardial infarction?

DEFF Research Database (Denmark)

Möller, J; Hallqvist, J; Diderichsen, Finn

1999-01-01

Our objectives were to study anger as a trigger of acute myocardial infarction (MI) and to explore potential effect modification by usual behavioral patterns related to hostility.......Our objectives were to study anger as a trigger of acute myocardial infarction (MI) and to explore potential effect modification by usual behavioral patterns related to hostility....

Artery of Percheron infarction after endoscopic pituitary surgery.

Science.gov (United States)

Aryan, Saritha; Thakar, Sumit; Hegde, A S

2016-10-01

Infarction in the artery of Percheron territory is a rare phenomenon in which occlusion of an unpaired perforating artery arising from the P1 segment on one side results in infarcts in the bilateral paramedian thalami with or without midbrain infarcts. We describe the case of a 40-year-old male who developed this complication following re-exploratory trans-sphenoidal surgery for a pituitary adenoma. In this first report of its kind in endoscopic pituitary surgery, the pathogenesis and clinico-radiological features of this rare vascular event are discussed.

Echocardiography diagnosis of myocardial infarction complications

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N.D. Oryshchyn

2016-03-01

Full Text Available Diagnosis and management of myocardial infarction complications are discussed in this article. These complications are associated with high level of mortality and surgery is a main treatment method. High level of suspicion and early diagnosis are essential for appropriate treatment and improvement of prognosis. Echocardiography is a main diagnostic method. Analysis of literature about contemporary management of mechanical complications of myocardial infarction has been performed, case reports are presented.

Hyperfixation of Tc-99m ECD in subacute cortical infarction

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Kim, Jae Seung; Kweon, Sun Uck; Ryu, Jin Sook; Moon, Dae Hyuk; Lee, Hee Kyung [College of Medicine, Ulsan Univ., Seoul (Korea, Republic of)

2001-07-01

It has been known that hyperfixation of Tc-99m ECD (HF) is not shown in subacute cerebral infarction because the brain distribution of Tc-99m ECD reflects not only perfusion but also the metabolic status of brain tissue. However, we observed several cases with HF in the subacute pure cortical infarction. To find out the cause of HF in subacute cortical infarction. We assessed the difference in associated cerebral hemodynamics and clinical findings between the subacute cortical infarctions with and without HF. We reviewed 16 patients (63.8{+-}8.6 yr, M/F: 15/1) with pure cortical infarction not involving adjacent subcortical white matter on MRI. All patients underwent acetazolamide stress brain perfusion SPECT using Tc-99m ECD and MRI at subacute period (7.3{+-}4.4 days from ictus). Uptake of Tc-99m ECD in infarcted cortex was assessed visually comparing the contralateral side. To assess the difference in associate clinical findings between the infarctions with and without HF, rCVR of the cerebral territory including infarcted cortex, extent of Gd-enhancement on MRI. Intervals between SPECT and ictus, and the presence of associated ICA stenosis were evaluated. Infarctions were focal (n=8) or multifocal (n=8) and located in frontoparietal cortices on MRI. Twelve patients were accompanied with ipsilateral ICA stenosis. Resting SPECT showed increased cortical uptake (=HF) in 7 patients and decreased in 9. rCVR of the MCA territory was preserved in all of the 7 patients with HF, compared with 4 of the 9 patients without HF (p=0.03). Gd-enhancement was minimal in all of the 7 patients with HF, compared with of the 0 patients without HF (p=0.03). Presence of ipsilateral ICA stenosis and intervals from ictus were not different (p>0.1) Subacute cerebral cortical infarction with HF was more frequently associated with preserved rCVR and minimal destruction of the blood-brain barrier than that without HF. Our findings suggest that HF may result from luxury perfusion of

Beyond textbook neuroanatomy: The syndrome of malignant PCA infarction.

Science.gov (United States)

Gogela, Steven L; Gozal, Yair M; Rahme, Ralph; Zuccarello, Mario; Ringer, Andrew J

2015-01-01

Given its limited vascular territory, occlusion of the posterior cerebral artery (PCA) usually does not result in malignant infarction. Challenging this concept, we present 3 cases of unilateral PCA infarction with secondary malignant progression, resulting from extension into what would classically be considered the posterior middle cerebral artery (MCA) territory. Interestingly, these were true PCA infarctions, not "MCA plus" strokes, since the underlying occlusive lesion was in the PCA. We hypothesize that congenital and/or acquired variability in the distribution and extent of territory supplied by the PCA may underlie this rare clinical entity. Patients with a PCA infarction should thus be followed closely and offered early surgical decompression in the event of malignant progression.

Prognostic significance of MR angiography in patients with cerebral infarction

International Nuclear Information System (INIS)

Moon, Woong Jae; Kim, Jun Ho; Seo, Jeong Jin; Cho, Ki Hyun; Kim, Yun Hyeon; Kim, Jae Kyu; Kang, Heoung Keun

1994-01-01

This study was designed to evaluate the prognostic significance of Magnetic resonance angiography(MRA) in patients with cerebral infarction. Magnetic Resonance Imaging(MRI) and 2 dimensional or 3 dimensional Time-of-Flight MRA were performed subsequently in 83 patients with cerebral infarction proven by brain CT and clinical manifestations, using GE Signa Advantage 1.5 T. We classified the size of infarction on MRI as Extent I( 6 cm) and classified the intracranial vascular occlusion according to visualizations of intracranial vascular branches on MRA as Grade 0, Grade I, Grade II, Grade III. And we evaluated clinical outcomes of these patients according to Rankin's disability scale, compared with MRI and MRA. In 72 cases(86.8%), the larger the size of infarction on MRI, the more severe vascular occlusion on MRA, the worse the clinical outcomes were noted(p < 0.01). However, in 7 cases(8.4%) who showed huge cerebral infarction on MRI with low grade intracranial vascular occlusion on MRA, the clinical outcomes were improved. In 4 cases(4.8%) who noted small sized cerebral infarction on MRI with high grade vascular occlusion on MRA, the clinical outcomes were worsened. MRA provides additional useful information to that provided by MRI in predicting the prognosis of patients with cerebral infarction

Respiratory muscle endurance is limited by lower ventilatory efficiency in post-myocardial infarction patients

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Laura M. T. Neves

2014-03-01

Full Text Available Background: Reduced respiratory muscle endurance (RME contributes to increased dyspnea upon exertion in patients with cardiovascular disease. Objective: The objective was to characterize ventilatory and metabolic responses during RME tests in post-myocardial infarction patients without respiratory muscle weakness. Method: Twenty-nine subjects were allocated into three groups: recent myocardial infarction group (RG, n=9, less-recent myocardial infarction group (LRG, n=10, and control group (CG, n=10. They underwent two RME tests (incremental and constant pressure with ventilatory and metabolic analyses. One-way ANOVA and repeated measures one-way ANOVA, both with Tukey post-hoc, were used between groups and within subjects, respectively. Results: Patients from the RG and LRG presented lower metabolic equivalent and ventilatory efficiency than the CG on the second (50± 06, 50± 5 vs. 42± 4 and third part (50± 11, 51± 10 vs. 43± 3 of the constant pressure RME test and lower metabolic equivalent during the incremental pressure RME test. Additionally, at the peak of the incremental RME test, RG patients had lower oxygen uptake than the CG. Conclusions : Post-myocardial infarction patients present lower ventilatory efficiency during respiratory muscle endurance tests, which appears to explain their inferior performance in these tests even in the presence of lower pressure overload and lower metabolic equivalent.

Neuroprotective effect of curcumin on transient focal cerebral ischemia in rats.

Science.gov (United States)

Zhao, Jing; Zhao, Yong; Zheng, Weiping; Lu, Yuyu; Feng, Gang; Yu, Shanshan

2008-09-10

Curcumin, a member of the curcuminoid family of compounds, is a yellow colored phenolic pigment obtained from the powdered rhizome of C. longa Linn. Recent studies have demonstrated that curcumin has protective effects against cerebral ischemia/reperfusion injury. However, little is known about its mechanism. Hence, in the present study the neuroprotective potential of curcumin was investigated in middle cerebral artery occlusion (MCAO) induced focal cerebral IR injury. Administration of curcumin 100 and 300 mg/kg i.p. 60 min after MCAO significantly diminished infarct volume, and improved neurological deficit in a dose-dependent manner. Nissl staining showed that the neuronal injury was significantly improved after being treated with curcumin. Curcumin significantly decreased the expression of caspase-3 protein. A higher number of TUNEL-positive cells were found in the vehicle group, but they were significantly decreased in the treated group. Taken together, these results suggest that the neuroprotective potentials of curcumin against focal cerebral ischemic injury are, at least in part, ascribed to its anti-apoptotic effects.

Estimation of myocardial infarct size by vectocardiography

International Nuclear Information System (INIS)

Takimiya, Akihiko

1987-01-01

Correlations between the vectorcardiogram (VCG) indice and infarct size (% defect) obtained from myocardial emission computed tomography with thallium-201 were studied in 45 patients with old infero-posterior myocardial infarction. The patients were divided into two groups, one consisting of eight patients who showed abnormal superior deviation of the QRS loop in a counterclockwise rotation beyond 30 msec in the frontal plane of VCG (referred to hereafter as CCW group), and another a non-CCW group consisting of 37 patients. The results obtained were as follows. (1) In the non-CCW group, there were significant negative correlations between the elevation and the Y-axial component of each instantaneous vector of the QRS loop at 30 msec, 35 msec, 40 msec, 45 msec, and between the Y-axial component of 50 msec instantaneous vector and the % defect. The correlation for both the elevation and the Y-axial component was closest at 40 msec, and there was most significantly close correlation between the elevation of 40 msec instantaneous vector and the % defect. (2) In the non-CCW group, there was also a significant correlation between the elevation of QRS area vector and the % defect. (3) In the CCW group, the infarct size could be estimated by the elevation of 30 msec instantaneous vector. An association with left anterior fascicular block was also indicated in the CCW group. (4) In infero-posterior myocardial infarction, the infarct size can be estimated using these VCG indices. (author)

Galectin-3 and post-myocardial infarction cardiac remodeling

NARCIS (Netherlands)

Meijers, Wouter C.; van der Velde, A. Rogier; Pascual-Figal, Domingo A.; de Boer, Rudolf A.

2015-01-01

This review summarizes the current literature regarding the involvement and the putative role(s) of galectin-3 in post-myocardial infarction cardiac remodeling. Post-myocardial infarction remodeling is characterized by acute loss of myocardium, which leads to structural and biomechanical changes in

Women's experiences and behaviour at onset of symptoms of ST segment elevation acute myocardial infarction

DEFF Research Database (Denmark)

Herning, Margrethe; Hansen, Peter R; Bygbjerg, B

2011-01-01

BACKGROUND: Minimizing time from onset of symptoms to treatment (treatment delay) is crucial for patients with ST segment elevation acute myocardial infarction (STEMI), and one of the great challenges is to reduce the delay relating to the prehospital behaviour of the patient (patient delay...

Risk and benefit of dual antiplatelet treatment among non-revascularized myocardial infarction patients in different age groups.

Science.gov (United States)

Juul, Nikolai; Gislason, Gunnar; Olesen, Jonas Bjerring; Lamberts, Morten; Hansen, Morten Lock; Karasoy, Deniz; Christiansen, Christine Benn; Torp-Pedersen, Christian; Sorensen, Rikke

2017-09-01

Dual anti-platelet treatment with clopidogrel and aspirin is indicated for most patients after myocardial infarction. We examined the risk/benefit relationship of dual anti-platelet treatment according to age in a nationwide cohort of 30,532 myocardial infarction patients without revascularization. Patients admitted with first-time myocardial infarction in 2002-2010, not undergoing revascularization, were identified from nationwide Danish registers. Dual anti-platelet treatment use was assessed by claimed prescriptions. Stratified into age groups, risk of bleeding, all-cause mortality and a combined endpoint of cardiovascular death, recurrent myocardial infarction and ischaemic stroke was analysed by Cox proportional-hazard models and tested in a propensity-score matched population. A total of 21,302 users and 9230 non-users of dual anti-platelet treatment were included (mean age 67.02 (±13.8) years and 64.7% males). Use of dual anti-platelet treatment decreased with age: 80% (79 years). We found a reduced risk of cardiovascular death, recurrent myocardial infarction and ischaemic stroke in users 79 years (HR=0.92; 95% CI 0.84-1.01, NS). Risk of bleeding increased with dual anti-platelet treatment use in patients aged 79 years (HR=1.46; 95% CI 1.22-1.74). Similar tendencies in all four age groups were found in the propensity-matched population. Dual anti-platelet treatment use was less likely among elderly patients although similar effects regarding both risk and benefit were found in all age groups. Increased focus on initiating dual anti-platelet treatment in elderly, non-invasively treated myocardial infarction patients is warranted.

Impact of pre-admission depression on mortality following myocardial infarction

DEFF Research Database (Denmark)

Sundbøll, Jens; Schmidt, Morten; Adelborg, Kasper

2017-01-01

BackgroundThe prognostic impact of previous depression on myocardial infarction survival remains poorly understood.AimsTo examine the association between depression and all-cause mortality following myocardial infarction.MethodUsing Danish medical registries, we conducted a nationwide population-...... in the depression definition.ConclusionsA history of depression was associated with a moderately increased all-cause mortality following myocardial infarction....

Bilateral cerebral hemispheric infarction associated with sildenafil citrate (Viagra) use.

Science.gov (United States)

Kim, K-K; Kim, D G; Ku, Y H; Lee, Y J; Kim, W-C; Kim, O J; Kim, H S

2008-03-01

Sildenafil citrate (Viagra) is one of the frequently prescribed drugs for men with erectile dysfunction. We describe a 52-year-old man with bilateral middle cerebral artery (MCA) territory infarction after sildenafil use. He ingested 100 mg of sildenafil and about 1 h later, he complained of chest discomfort, palpitation and dizziness followed by mental obtundation, global aphasia and left hemiparesis. Brain magnetic resonance imaging documented acute bilateral hemispheric infarction, and cerebral angiography showed occluded bilateral MCA. Despite significant bilateral MCA stenosis and cerebral infarction, systemic hypotension persisted for a day. We presume that cerebral infarction was caused by cardioembolism with sildenafil use.

Assessment of Myocardial Infarction by Cardiac Magnetic Resonance Imaging and Long-Term Mortality

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Petriz, João Luiz Fernandes, E-mail: jlpetriz@cardiol.br [Universidade Federal do Rio de Janeiro (UFRJ) / Instituto do Coração Edson Saad - Programa de Pós Graduação em Medicina (Cardiologia), Rio de Janeiro, RJ (Brazil); Hospital Barra D’Or, Rio de Janeiro, RJ (Brazil); Instituto D’Or de Pesquisa e Ensino, Rio de Janeiro, RJ (Brazil); Gomes, Bruno Ferraz de Oliveira; Rua, Braulio Santos [Hospital Barra D’Or, Rio de Janeiro, RJ (Brazil); Azevedo, Clério Francisco [Instituto D’Or de Pesquisa e Ensino, Rio de Janeiro, RJ (Brazil); Hadlich, Marcelo Souza [Universidade Federal do Rio de Janeiro (UFRJ) / Instituto do Coração Edson Saad - Programa de Pós Graduação em Medicina (Cardiologia), Rio de Janeiro, RJ (Brazil); Instituto D’Or de Pesquisa e Ensino, Rio de Janeiro, RJ (Brazil); Mussi, Henrique Thadeu Periard [Universidade Federal do Rio de Janeiro (UFRJ) / Instituto do Coração Edson Saad - Programa de Pós Graduação em Medicina (Cardiologia), Rio de Janeiro, RJ (Brazil); Hospital Barra D’Or, Rio de Janeiro, RJ (Brazil); Taets, Gunnar de Cunto [Instituto D’Or de Pesquisa e Ensino, Rio de Janeiro, RJ (Brazil); Nascimento, Emília Matos do; Pereira, Basílio de Bragança; Silva, Nelson Albuquerque de Souza e [Universidade Federal do Rio de Janeiro (UFRJ) / Instituto do Coração Edson Saad - Programa de Pós Graduação em Medicina (Cardiologia), Rio de Janeiro, RJ (Brazil)

2015-02-15

Cardiac magnetic resonance imaging provides detailed anatomical information on infarction. However, few studies have investigated the association of these data with mortality after acute myocardial infarction. To study the association between data regarding infarct size and anatomy, as obtained from cardiac magnetic resonance imaging after acute myocardial infarction, and long-term mortality. A total of 1959 reports of “infarct size” were identified in 7119 cardiac magnetic resonance imaging studies, of which 420 had clinical and laboratory confirmation of previous myocardial infarction. The variables studied were the classic risk factors – left ventricular ejection fraction, categorized ventricular function, and location of acute myocardial infarction. Infarct size and acute myocardial infarction extent and transmurality were analyzed alone and together, using the variable named “MET-AMI”. The statistical analysis was carried out using the elastic net regularization, with the Cox model and survival trees. The mean age was 62.3 ± 12 years, and 77.3% were males. During the mean follow-up of 6.4 ± 2.9 years, there were 76 deaths (18.1%). Serum creatinine, diabetes mellitus and previous myocardial infarction were independently associated with mortality. Age was the main explanatory factor. The cardiac magnetic resonance imaging variables independently associated with mortality were transmurality of acute myocardial infarction (p = 0.047), ventricular dysfunction (p = 0.0005) and infarcted size (p = 0.0005); the latter was the main explanatory variable for ischemic heart disease death. The MET-AMI variable was the most strongly associated with risk of ischemic heart disease death (HR: 16.04; 95%CI: 2.64-97.5; p = 0.003). The anatomical data of infarction, obtained from cardiac magnetic resonance imaging after acute myocardial infarction, were independently associated with long-term mortality, especially for ischemic heart disease death.

NOSH-NBP, a Novel Nitric Oxide and Hydrogen Sulfide- Releasing Hybrid, Attenuates Ischemic Stroke-Induced Neuroinflammatory Injury by Modulating Microglia Polarization

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Jing Ji

2017-05-01

Full Text Available NOSH-NBP, a novel nitric oxide (NO and hydrogen sulfide (H2S-releasing hybrid, protects brain from ischemic stroke. This study mainly aimed to investigate the therapeutic effect of NOSH-NBP on ischemic stroke and the underlying mechanisms. In vivo, transient middle cerebral artery occlusion (tMCAO was performed in C57BL/6 mice, with NO-NBP and H2S-NBP as controls. NO and H2S scavengers, carboxy-PTIO and BSS, respectively, were used to quench NO and H2S of NOSH-NBP. In vitro, BV2 microglia/BMDM were induced to the M1/2 phenotype, and conditioned medium (CM experiments in BV2 microglia, neurons and b.End3 cerebral microvascular endothelial cells (ECs were performed. Microglial/macrophage activation/polarization was assessed by flow cytometry, Western blot, RT-qPCR, and ELISA. Neuronal and EC survival was measured by TUNEL, flow cytometry, MTT and LDH assays. Transmission electron microscopy, EB extravasation, brain water content, TEER measurement and Western blot were used to detect blood–brain barrier (BBB integrity and function. Interestingly, NOSH-NBP significantly reduced cerebral infarct volume and ameliorated neurological deficit, with superior effects compared with NO-NBP and/or H2S-NBP in mice after tMCAO. Both NO and H2S-releasing groups contributed to protection by NOSH-NBP. Additionally, NOSH-NBP decreased neuronal death and attenuated BBB dysfunction in tMCAO-treated mice. Furthermore, NOSH-NBP promoted microglia/macrophage switch from an inflammatory M1 phenotype to the protective M2 phenotype in vivo and in vitro. Moreover, the TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome were involved in the inhibitory effects of NOSH-NBP on M1 polarization, while peroxisome proliferator activated receptor gamma signaling contributed to NOSH-NBP induced M2 polarization. These findings indicated that NOSH-NBP is a potential therapeutic agent that preferentially promotes microglial/macrophage M1–M2 switch in ischemic stroke.

Spontaneous resolution of splenic infarcts after distal splenorenal ...

African Journals Online (AJOL)

Background: In cases of portal hypertension with splenic infarcts, splenectomy with proximal splenorenal shunt has been recommended. We are sharing our experience with distal splenorenal shunt in these cases contrary to the popular belief. Materials and Methods: Splenic infarcts were graded as mild, moderate and ...

Clinical values of CT and dynamic CT in brain infarction

International Nuclear Information System (INIS)

Lim, Soo Il; Jang, Do; Seo, Eun Joo; Sohn, Myung Hee; Choi, Ki Chul

1985-01-01

With the advent of faster scan time and new computer program, a scanning technique called 'dynamic computed tomography' has become possible. Dynamic computed tomography consisted of performing multiple rapid sequence scans after injection of contrast material. The authors have evaluated the clinical usefulness of computed tomography and dynamic computed tomography of 93 patients with brain infarction and/or ischemia during the period of 17 months from April 1983 to August 1984 in Department of Radiology, Chonbuk National University Hospital. The results were as follows; 1. The age distribution ranged from 18 years to 78 years. Among them the most common age group was between 50 years and 59 years (40.9%). 2. The sites of brain infarction were cerebral lobes (63 cases,68), basal ganglia (15 cases, 16.1%) and multiple sites (6 cases, 6.4%). The common affected site was middle cerebral artery territories. 3. The contrast enhancement of acute infarction was noted in 14 cases (17.5%) which occurred commonly between 3 days and 2 weeks from ictus. 4. The patterns of time-density curve in brain infarction and/or ischemia were as follow: a. Depression of slow wash-in phase was 20 cases (59%). b. Lower peak concentration was 17 cases (50%). c. Lower and delayed peak concentration was 7 cases (21%). d. No definite peak concentration was 6 cases (18%). First three patterns of time-density curve were thought as relatively characteristic curve of brain infarction and/or ischemia. 5. Two cases that showed negative findings on precontrast CT scan appeared to be positive findings as hypodensity on postcontrast CT scan and were confirmed as brain infarction by dynamic CT. 6. The diagnostic entity of dynamic CT scan were as follows; a. large artery thrombotic infarction were 23 cases (58%). b. lacnar infarction were 6 cases (15%). c. ischemia were 5 cases (13%). d. normal were 5 cases (13%). In six cases of lacunar infarction which was double hypodensity on pre-and postcontrast CT

Clinical values of CT and dynamic CT in brain infarction

Energy Technology Data Exchange (ETDEWEB)

Lim, Soo Il; Jang, Do; Seo, Eun Joo; Sohn, Myung Hee; Choi, Ki Chul [Chonbuk National University College of Medicine, Jeonju (Korea, Republic of)

1985-04-15

With the advent of faster scan time and new computer program, a scanning technique called 'dynamic computed tomography' has become possible. Dynamic computed tomography consisted of performing multiple rapid sequence scans after injection of contrast material. The authors have evaluated the clinical usefulness of computed tomography and dynamic computed tomography of 93 patients with brain infarction and/or ischemia during the period of 17 months from April 1983 to August 1984 in Department of Radiology, Chonbuk National University Hospital. The results were as follows; 1. The age distribution ranged from 18 years to 78 years. Among them the most common age group was between 50 years and 59 years (40.9%). 2. The sites of brain infarction were cerebral lobes (63 cases,68), basal ganglia (15 cases, 16.1%) and multiple sites (6 cases, 6.4%). The common affected site was middle cerebral artery territories. 3. The contrast enhancement of acute infarction was noted in 14 cases (17.5%) which occurred commonly between 3 days and 2 weeks from ictus. 4. The patterns of time-density curve in brain infarction and/or ischemia were as follow: a. Depression of slow wash-in phase was 20 cases (59%). b. Lower peak concentration was 17 cases (50%). c. Lower and delayed peak concentration was 7 cases (21%). d. No definite peak concentration was 6 cases (18%). First three patterns of time-density curve were thought as relatively characteristic curve of brain infarction and/or ischemia. 5. Two cases that showed negative findings on precontrast CT scan appeared to be positive findings as hypodensity on postcontrast CT scan and were confirmed as brain infarction by dynamic CT. 6. The diagnostic entity of dynamic CT scan were as follows; a. large artery thrombotic infarction were 23 cases (58%). b. lacnar infarction were 6 cases (15%). c. ischemia were 5 cases (13%). d. normal were 5 cases (13%). In six cases of lacunar infarction which was double hypodensity on pre

Evaluation of radioactive potassium and its analogues for imaging myocardial infarcts

International Nuclear Information System (INIS)

Gorten, R.J.

1977-01-01

An extensive clinical evaluation was undertaken to assess the value of myocardial infarct imaging with radioactive potassium and analogues. Of 130 patients so examined, 80 were diagnosed as having suffered infarcts in the recent or distant past on the basis of all information other than the scan. The radionuclide imaging results were abnormal in 87.5 percent overall, 97 percent in acute transmural infarcts, and 83 percent in lesions over 3 weeks old. In 50 patients not considered to have had myocardial infarcts or contusions, apparently false abnormal results were obtained in 15 percent. These were all patients in whom additional diagnostic help was desired after the ordinary laboratory tests and electrocardiograms. Excellent agreement of infarct location was discovered on comparing radionuclide scans with radiographic contrast ventriculography. On comparing electrocardiograms with scans for infarct location, 85 percent complete or partial correlation was revealed. Agreement between scan abnormalities and significant-appearing coronary arteriographic lesions was rather poor, causing one to realize that 43 K scan abnormalities indicate regions of poor blood extraction by old or recent infarcts, rather than just poor regional arterial perfusion. While costly, radionuclide scans often provide worthwhile information about presence or absence of infarcts as well as about their location and size. Electrocardiograms and blood enzyme levels each cost less, but are almost always performed in serial fashion. This makes them actually more expensive than a single scan. Furthermore, a normal scan in a patient being considered for acute coronary care may be used as potent argument against the presence of an infarct, thereby saving costly intensive care and monitoring

Clinical menifestations and CT findings of lacunar infarction

International Nuclear Information System (INIS)

Shimada, Tsutomu; Kaneko, Mitsuo; Tanaka, Keisei; Sato, Kengo; Yamamoto, Toshiki

1983-01-01

Since the introduction of the CT scanner, the present authors have experienced 111 cases of lacunar infarction which were diagnosed on the basis of clinical manifestations and/or CT findings, being 35 % of total 318 cases of acute cerebral infarction in our series. The clinical features and their correlation with the CT findings were studied in the cases of lacunar infarction. The results were as follows. 1) Seventy-four per cent of the patients were hypertensive. 2) Fifty per cent of the patients had only motor deficit. 3) The patients who revealed small deep infarctions in the posterior two-thirds of the posterior limb of the internal capsule on CT scan had more marked motor impariment with more involvement of the upper extremity than the lower extremity. 4) The recovery of the motor deficit was generally good, but unsatisfactory when the patient had a larger lesion than 10 mm in diameter. (author)

Matrix Signaling Subsequent to a Myocardial Infarction

Directory of Open Access Journals (Sweden)

Derrick Akpalu

2017-10-01

Full Text Available This study investigated the release and proteomic profile of tissue factor microparticles (TFMPs prospectively (up to 6 months following a myocardial infarction (MI in a chronic porcine model to establish their utility in tracking cellular level activities that predict physiologic outcomes. Our animal groups (n = 6 to 8 each consisted of control, noninfarcted (negative control; infarcted only (positive control; and infarcted animals treated with cardiac resynchronization therapy (CRT and a β-blocker (BB (metoprolol succinate. The authors found different protein profiles in TFMPs between the control, infarcted only group, and the CRT + BB treated group with predictive impact on the outward phenotype of pathological remodeling after an MI within and between groups. This novel approach of monitoring cellular level activities by profiling the content of TFMPs has the potential of addressing a shortfall of the current crop of cardiac biomarkers, which is the inability to capture composite molecular changes associated with chronic maladaptive signaling in a spatial and temporal manner.

Exercise induced ST elevation and residual myocardial ischemia in previous myocardial infarction

International Nuclear Information System (INIS)

Shimonagata, Tsuyoshi; Nishimura, Tsunehiko; Uehara, Toshiisa; Hayashida, Kohei; Saito, Muneyasu; Sumiyoshi, Tetsuya

1987-01-01

The purpose of this study was to evaluate the clinical significance of stress induced ST elevation on infarcted area in 65 patients with previous myocardial infarction (single vessel disease) who had stress thallium scan. Stress induced ST changes on infarcted area were compared with quantitative assessment of myocardial ischemia (thallium ischemic score; TIS) and extent of myocardial infarction (defect score; DS) derived from circumferential profile analysis. In patients with previous myocardial infarction in less than 3 month from the onset (n = 36), left ventricular ejection fraction (LVEF) and extent of abnormal LV wall motion were not significantly different between patients with stress induced ST elevation ( ≥ 2 mm, n = 26) and those with stress induced ST elevation ( < 2 mm, n = 10), while, in patients with previous myocardial infarction in more than 3 month (n = 29), patients with stress induced ST elevation ( ≥ 2 mm, n = 15) showed left ventricular dyskinesis more frequently than those with ST elevation ( < 2 mm, n = 14). In addition, the former showed significantly higher DS and significantly lower TIS than the latter. In patients with previous myocardial infarction in less than 3 month, patients with ST elevation ( ≥ 2 mm, n = 15) with prominent upright T wave (n = 15) had transient thallium defect in infarcted area in 73 % and they had significantly higher LVEF and TIS than those with ST elevation ( < 2 mm, n = 11). These results indicated that ST elevation in infarcted area reflect different significance according to the recovery of injured myocardium and stress induced ST elevation with prominent upright T wave in infarcted area reflect residual myocardial ischemia in less than 3 month from the onset of myocardial infarction. (author)

Free radical scavenger, edaravone, reduces the lesion size of lacunar infarction in human brain ischemic stroke

Science.gov (United States)

2011-01-01

Background Although free radicals have been reported to play a role in the expansion of ischemic brain lesions, the effect of free radical scavengers is still under debate. In this study, the temporal profile of ischemic stroke lesion sizes was assessed for more than one year to evaluate the effect of edaravone which might reduce ischemic damage. Methods We sequentially enrolled acute ischemic stroke patients, who admitted between April 2003 and March 2004, into the edaravone(-) group (n = 83) and, who admitted between April 2004 and March 2005, into the edaravone(+) group (n = 93). Because, edaravone has been used as the standard treatment after April 2004 in our hospital. To assess the temporal profile of the stroke lesion size, the ratio of the area [T2-weighted magnetic resonance images (T2WI)/iffusion-weighted magnetic resonance images (DWI)] were calculated. Observations on T2WI were continued beyond one year, and observational times were classified into subacute (1-2 months after the onset), early chronic (3-6 month), late chronic (7-12 months) and old (≥13 months) stages. Neurological deficits were assessed by the National Institutes of Health Stroke Scale upon admission and at discharge and by the modified Rankin Scale at 1 year following stroke onset. Results Stroke lesion size was significantly attenuated in the edaravone(+) group compared with the edaravone(-) group in the period of early and late chronic observational stages. However, this reduction in lesion size was significant within a year and only for the small-vessel occlusion stroke patients treated with edaravone. Moreover, patients with small-vessel occlusion strokes that were treated with edaravone showed significant neurological improvement during their hospital stay, although there were no significant differences in outcome one year after the stroke. Conclusion Edaravone treatment reduced the volume of the infarct and improved neurological deficits during the subacute period, especially

Free radical scavenger, edaravone, reduces the lesion size of lacunar infarction in human brain ischemic stroke

Directory of Open Access Journals (Sweden)

Suzuki Akifumi

2011-03-01

Full Text Available Abstract Background Although free radicals have been reported to play a role in the expansion of ischemic brain lesions, the effect of free radical scavengers is still under debate. In this study, the temporal profile of ischemic stroke lesion sizes was assessed for more than one year to evaluate the effect of edaravone which might reduce ischemic damage. Methods We sequentially enrolled acute ischemic stroke patients, who admitted between April 2003 and March 2004, into the edaravone(- group (n = 83 and, who admitted between April 2004 and March 2005, into the edaravone(+ group (n = 93. Because, edaravone has been used as the standard treatment after April 2004 in our hospital. To assess the temporal profile of the stroke lesion size, the ratio of the area [T2-weighted magnetic resonance images (T2WI/iffusion-weighted magnetic resonance images (DWI] were calculated. Observations on T2WI were continued beyond one year, and observational times were classified into subacute (1-2 months after the onset, early chronic (3-6 month, late chronic (7-12 months and old (≥13 months stages. Neurological deficits were assessed by the National Institutes of Health Stroke Scale upon admission and at discharge and by the modified Rankin Scale at 1 year following stroke onset. Results Stroke lesion size was significantly attenuated in the edaravone(+ group compared with the edaravone(- group in the period of early and late chronic observational stages. However, this reduction in lesion size was significant within a year and only for the small-vessel occlusion stroke patients treated with edaravone. Moreover, patients with small-vessel occlusion strokes that were treated with edaravone showed significant neurological improvement during their hospital stay, although there were no significant differences in outcome one year after the stroke. Conclusion Edaravone treatment reduced the volume of the infarct and improved neurological deficits during the subacute

Acute myocardial infarction mortality in Cuba, 1999-2008.

Science.gov (United States)

Armas, Nurys B; Ortega, Yanela Y; de la Noval, Reinaldo; Suárez, Ramón; Llerena, Lorenzo; Dueñas, Alfredo F

2012-10-01

Acute myocardial infarction is one of the leading causes of death in the world. This is also true in Cuba, where no national-level epidemiologic studies of related mortality have been published in recent years. Describe acute myocardial infarction mortality in Cuba from 1999 through 2008. A descriptive study was conducted of persons aged ≥25 years with a diagnosis of acute myocardial infarction from 1999 through 2008. Data were obtained from the Ministry of Public Health's National Statistics Division database for variables: age; sex; site (out of hospital, in hospital or in hospital emergency room) and location (jurisdiction) of death. Proportions, age- and sex-specific rates and age-standardized overall rates per 100,000 population were calculated and compared over time, using the two five-year time frames within the study period. A total of 145,808 persons who had suffered acute myocardial infarction were recorded, 75,512 of whom died, for a case-fatality rate of 51.8% (55.1% in 1999-2003 and 49.7% in 2004-2008). In the first five-year period, mortality was 98.9 per 100,000 population, falling to 81.8 per 100,000 in the second; most affected were people aged ≥75 years and men. Of Cuba's 14 provinces and special municipality, Havana, Havana City and Camagüey provinces, and the Isle of Youth Special Municipality showed the highest mortality; Holguín, Ciego de Ávila and Granma provinces the lowest. Out-of-hospital deaths accounted for the greatest proportion of deaths in both five-year periods (54.8% and 59.2% in 1999-2003 and 2004-2008, respectively). Although risk of death from acute myocardial infarction decreased through the study period, it remains a major health problem in Cuba. A national acute myocardial infarction case registry is needed. Also required is further research to help elucidate possible causes of Cuba's high acute myocardial infarction mortality: cardiovascular risk studies, studies of out-of-hospital mortality and quality of care