WorldWideScience

Sample records for accentuates ethanol-induced myocardial

  1. Alcohol Dehydrogenase Accentuates Ethanol-Induced Myocardial Dysfunction and Mitochondrial Damage in Mice: Role of Mitochondrial Death Pathway

    GUO Rui; Ren, Jun

    2010-01-01

    Objectives Binge drinking and alcohol toxicity are often associated with myocardial dysfunction possibly due to accumulation of the ethanol metabolite acetaldehyde although the underlying mechanism is unknown. This study was designed to examine the impact of accelerated ethanol metabolism on myocardial contractility, mitochondrial function and apoptosis using a murine model of cardiac-specific overexpression of alcohol dehydrogenase (ADH). Methods ADH and wild-type FVB mice were acutely chall...

  2. Aldehyde Dehydrogenase 2 Knockout Accentuates Ethanol-Induced Cardiac Depression: Role of Protein Phosphatases

    Ma, Heng; Byra, Emily A.; Yu, Lu; Hu, Nan; Kitagawa, Kyoko; Nakayama, Keiichi I.; Kawamoto, Toshihiro; Ren, Jun

    2010-01-01

    Alcohol consumption leads to myocardial contractile dysfunction possibly due to the toxicity of ethanol and its major metabolite acetaldehyde. This study was designed to examine the influence of mitochondrial aldehyde dehydrogenase-2 (ALDH2) knockout (KO) on acute ethanol exposure-induced cardiomyocyte dysfunction. Wild-type (WT) and ALDH2 KO mice were subjected to acute ethanol (3 g/kg, i.p.) challenge and cardiomyocyte contractile function was assessed 24 hrs later using an IonOptix® edge-d...

  3. Involvement of AMPK in Alcohol Dehydrogenase Accentuated Myocardial Dysfunction Following Acute Ethanol Challenge in Mice

    GUO Rui; Scott, Glenda I.; Ren, Jun

    2010-01-01

    Objectives Binge alcohol drinking often triggers myocardial contractile dysfunction although the underlying mechanism is not fully clear. This study was designed to examine the impact of cardiac-specific overexpression of alcohol dehydrogenase (ADH) on ethanol-induced change in cardiac contractile function, intracellular Ca2+ homeostasis, insulin and AMP-dependent kinase (AMPK) signaling. Methods ADH transgenic and wild-type FVB mice were acutely challenged with ethanol (3 g/kg/d, i.p.) for 3...

  4. Ethanol-induced alterations in sup 14 C-glucose utilization: Modulation by brain adenosine in mice

    Anwer, J.; Dar, M.S. (East Carolina Univ., Greenville, NC (United States))

    1992-02-26

    The possible role of brain adenosine (Ado) in acute ethanol-induced alteration in glucose utilization in the cerebellum and brain stem was investigated. The slices were incubated for 100 min in a glucose medium in Warburg flasks using {sup 14}C-glucose as a tracer. Trapped {sup 14}CO{sub 2} was counted to estimate glucose utilization. Ethanol markedly increased the glucose utilization in both areas of brain. Theophylline, an Ado antagonist, significantly reduced ethanol-induced increase in glucose utilization in both brain areas. Ado agonist CHA significantly accentuated ethanol-induced increase in glucose utilization in both motor areas. Ado agonist CHA significantly accentuated ethanol-induced increase in glucose utilization in both motor areas. Ethanol was still able to produce a smaller but significant increase in glucose utilization in both brain areas when theophylline and CHA were given together, suggesting an additional mechanism. Collectively, the data indicate that ethanol-induced glucose utilization in the cerebellum and brain stem is modulated by brain Ado receptor and by non-adenosinergic mechanism.

  5. Lithium protects ethanol-induced neuronal apoptosis

    Lithium is widely used for the treatment of bipolar disorder. Recent studies have demonstrated its neuroprotective effect. Ethanol is a potent neurotoxin that is particularly harmful to the developing nervous system. In this study, we evaluated lithium's neuroprotection against ethanol-induced apoptosis. Transient exposure of infant mice to ethanol caused apoptotic cell death in brain, which was prevented significantly by administering a low dose of lithium 15 min later. In cultured cerebellar granule neurons, ethanol-induced apoptosis and activation of caspase-3/9, both of which were prevented by lithium. However, lithium's protection is not mediated by its commonly known inhibition of glycogen synthase3β, because neither ethanol nor lithium has significant effects on the phosphorylation of Akt (ser473) or GSK3β (ser9). In addition, the selective GSK-3β inhibitor SB-415286 was unable to prevent ethanol-induced apoptosis. These data suggest lithium may be used as a potential preventive measure for ethanol-induced neurological deficits

  6. Ethanol-induced oxidative stress: basic knowledge

    Comporti, Mario; Signorini, Cinzia; Leoncini, Silvia; Gardi, Concetta; Ciccoli, Lucia; Giardini, Anna; Vecchio, Daniela; Arezzini, Beatrice

    2009-01-01

    After a general introduction, the main pathways of ethanol metabolism (alcohol dehydrogenase, catalase, coupling of catalase with NADPH oxidase and microsomal ethanol-oxidizing system) are shortly reviewed. The cytochrome P450 isoform (CYP2E1) specifically involved in ethanol oxidation is discussed. The acetaldehyde metabolism and the shift of the NAD/NADH ratio in the cellular environment (reductive stress) are stressed. The toxic effects of acetaldehyde are mentioned. The ethanol-induced ox...

  7. The effect of accentuation on vowel recognition

    Braun, Bettina; Koreman, Jacques; Trouvain, Jürgen

    2001-01-01

    This study focuses on the implementation of the phonetic effects of vowel accentuation in automatic speech recognition (ASR). The durational and spectral effects of accentuation are investigated separately by manipulating the transition and observation probabilities in hidden Markov models. We also attempt to implement the undershoot hypothesis [1], which describes spectral reduction as a direct consequence of shortening. Our findings support the widespread belief that the transition probabil...

  8. Preventive effects of geranylgeranylacetone on rat ethanol-induced gastritis

    Ning, Jian-Wen; Lin, Guan-Bin; Ji, Feng; Xu, Jia; Sharify, Najeeb

    2012-01-01

    AIM: To establish a rat ethanol gastritis model, we evaluated the effects of ethanol on gastric mucosa and studied the preventive effects of geranylgeranylacetone on ethanol-induced chronic gastritis.

  9. ETHANOL-INDUCED LOCOMOTOR ACTIVITY IN ADOLESCENT RATS AND THE RELATIONSHIP WITH ETHANOL-INDUCED CONDITIONED PLACE PREFERENCE AND CONDITIONED TASTE AVERSION

    Acevedo, María Belén; Nizhnikov, Michael E.; Norman E. Spear; Molina, Juan C.; Pautassi, Ricardo Marcos

    2012-01-01

    Adolescent rats exhibit ethanol-induced locomotor activity (LMA), which is considered an index of ethanol’s motivational properties likely to predict ethanol self-administration, but few studies have reported or correlated ethanol-induced LMA with conditioned place preference by ethanol at this age. The present study assessed age-related differences in ethanol’s motor stimulating effects and analysed the association between ethanol-induced LMA and conventional measures of ethanol-induced rein...

  10. The Analysis of Low Accentuation in Estonian

    Asu, Eva Liina; Nolan, Francis

    2007-01-01

    In Estonian, as in a number of other languages, the nuclear pitch accent is often low and level. This paper presents two studies of this phenomenon. The first, a phonetic analysis of carefully structured read sentences shows that low accentuation can also spread to the prenuclear accents in an intonational phrase. The resulting sentence contours…

  11. Recovery of Saccharomyces cerevisiae from ethanol-induced growth inhibition.

    Walker-Caprioglio, H M; Rodriguez, R J; Parks, L. W.

    1985-01-01

    Ethanol caused altered mobility of the lipophilic probe 1,6-diphenyl-1,3,5-hexatriene in plasma membrane preparations of Saccharomyces cerevisiae. Because lipids had been shown to protect yeast cells against ethanol toxicity, sterols, fatty acids, proteins, and combinations of these were tested; however, protection from growth inhibition was not seen. Ethanol-induced, prolonged lag periods and diminished growth rates in S. cerevisiae were reduced by an autoconditioning of the medium by the in...

  12. Diosmin protects against ethanol-induced gastric injury in rats: novel anti-ulcer actions.

    Hany H Arab

    Full Text Available Alcohol consumption has been commonly associated with gastric mucosal lesions including gastric ulcer. Diosmin (DIO is a natural citrus flavone with remarkable antioxidant and anti-inflammatory features that underlay its protection against cardiac, hepatic and renal injuries. However, its impact on gastric ulcer has not yet been elucidated. Thus, the current study aimed to investigate the potential protective effects of DIO against ethanol-induced gastric injury in rats. Pretreatment with DIO (100 mg/kg p.o. attenuated the severity of ethanol gastric mucosal damage as evidenced by lowering of ulcer index (UI scores, area of gastric lesions, histopathologic aberrations and leukocyte invasion. These actions were analogous to those exerted by the reference antiulcer sucralfate. DIO suppressed gastric inflammation by curbing of myeloperoxidase (MPO and tumor necrosis factor-α (TNF-α levels along with nuclear factor kappa B (NF-κB p65 expression. It also augmented the anti-inflammatory interleukin-10 (IL-10 levels. Meanwhile, DIO halted gastric oxidative stress via inhibition of lipid peroxides with concomitant enhancement of glutathione (GSH, glutathione peroxidase (GPx and the total antioxidant capacity (TAC. With respect to gastric mucosal apoptosis, DIO suppressed caspase-3 activity and cytochrome C (Cyt C with enhancement of the anti-apoptotic B cell lymphoma-2 (Bcl-2 in favor of cell survival. These favorable actions were associated with upregulation of the gastric cytoprotective prostaglandin E2 (PGE2 and nitric oxide (NO. Together, these findings accentuate the gastroprotective actions of DIO in ethanol gastric injury which were mediated via concerted multi-pronged actions, including suppression of gastric inflammation, oxidative stress and apoptosis besides boosting of the antioxidant and the cytoprotective defenses.

  13. Central adenosinergic system involvement in ethanol-induced motor incoordination in mice

    To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. adenosine agonists, N6-(R-phenylisopropyl)adenosine (R-PIA), N6-(S-phenylisopropyl)adenosine, 5'-(N-cyclopropyl)-carboxamidoadenosine, antagonists, theophylline and 8-p-(sulfophenyl)theophylline as well as enprofylline on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod. Adenosine agonists and antagonists dose dependently accentuated and attenuated, respectively, ethanol-induced motor incoordination, thereby suggesting a central mechanism of adenosine modulation of this effect of ethanol and confirmed our previous reports in which adenosine agonists and antagonists were given i.p. Enprofylline, a weak adenosine antagonist but potent inhibitor of cyclic AMP phosphodiesterase, did not alter ethanol's motor incoordination, further supporting involvement of brain adenosine receptor mechanism(s) in ethanol-adenosine interactions. Results from R-PIA and N6-(S-phenylisopropyl)adenosine experiments showed nearly a 40-fold greater potency of R-vs. S-diastereoisomer, suggesting predominance of adenosine A1 subtype. However, 5'-(N-cyclopropyl)-carboxamidoadenosine data indicate complexity of the mechanism(s) and point toward an additional involvement of a yet unknown subtype of adenosine A2. No effect of ethanol on blood or brain levels of [3H]R-PIA was noted and sufficient amount of the latter entered the brain to suggest adenosine receptor activation adequate to produce behavioral interaction with ethanol. There was no escape of i.c.v.-administered [3H]R-PIA from brain to the peripheral circulation ruling out a peripheral and supporting a central mechanism of ethanol-adenosine interaction

  14. Central adenosinergic system involvement in ethanol-induced motor incoordination in mice

    Dar, M.S. (East Carolina Univ., Greenville, NC (USA))

    1990-12-01

    To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. adenosine agonists, N6-(R-phenylisopropyl)adenosine (R-PIA), N6-(S-phenylisopropyl)adenosine, 5'-(N-cyclopropyl)-carboxamidoadenosine, antagonists, theophylline and 8-p-(sulfophenyl)theophylline as well as enprofylline on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod. Adenosine agonists and antagonists dose dependently accentuated and attenuated, respectively, ethanol-induced motor incoordination, thereby suggesting a central mechanism of adenosine modulation of this effect of ethanol and confirmed our previous reports in which adenosine agonists and antagonists were given i.p. Enprofylline, a weak adenosine antagonist but potent inhibitor of cyclic AMP phosphodiesterase, did not alter ethanol's motor incoordination, further supporting involvement of brain adenosine receptor mechanism(s) in ethanol-adenosine interactions. Results from R-PIA and N6-(S-phenylisopropyl)adenosine experiments showed nearly a 40-fold greater potency of R-vs. S-diastereoisomer, suggesting predominance of adenosine A1 subtype. However, 5'-(N-cyclopropyl)-carboxamidoadenosine data indicate complexity of the mechanism(s) and point toward an additional involvement of a yet unknown subtype of adenosine A2. No effect of ethanol on blood or brain levels of (3H)R-PIA was noted and sufficient amount of the latter entered the brain to suggest adenosine receptor activation adequate to produce behavioral interaction with ethanol. There was no escape of i.c.v.-administered (3H)R-PIA from brain to the peripheral circulation ruling out a peripheral and supporting a central mechanism of ethanol-adenosine interaction.

  15. Ethanol induces rotational behavior in 6-hydroxydopamine lesioned mice

    Silverman, P.B.

    1987-03-09

    Mice with unilateal striatal lesions created by 6-hydroxydopamine (6HDA) injection were screened for rotational (circling) behavior in response to injection of amphetamine and apomorphine. Those that rotated ipsilaterally in response to amphetamine and contralaterally in response to apomorphine were subsequently challenged with 1 to 3 g/kg (i.p.) ethanol. Surprisingly, ethanol induced dose related contralateral (apomorphine-like) rotation which, despite gross intoxication, was quite marked in most animals. No significant correlation was found between the number of turns made following ethanol and made after apomorphine or amphetamine. 14 references, 2 figures, 1 table.

  16. Ethanol-induced hepatic autophagy: Friend or foe?

    2015-01-01

    Excessive alcohol intake may induce hepatic apoptosis,steatosis, fibrosis, cirrhosis and even cancer. Ethanolinducedactivation of general or selective autophagyas mitophagy or lipophagy in hepatocytes is generallyconsidered a prosurvival mechanism. On the otherside of the coin, upregulation of autophagy in nonhepatocytesas stellate cells may stimulate fibrogenesisand subsequently induce detrimental effects on the liver.The autophagic response of other non-hepatocytes asmacrophages and endothelial cells is unknown yet andneeds to be investigated as these cells play importantroles in ethanol-induced hepatic steatosis and damage.Selective pharmacological stimulation of autophagyin hepatocytes may be of therapeutic importance inalcoholic liver disease.

  17. Early role of the κ opioid receptor in ethanol-induced reinforcement

    Pautassi, Ricardo Marcos; Nizhnikov, Michael E.; Acevedo, Ma. Belén; Norman E. Spear

    2012-01-01

    Effects of early ethanol exposure on later ethanol intake emphasize the importance of understanding the neurobiology of ethanol-induced reinforcement early in life. Infant rats exhibit ethanol-induced appetitive conditioning and ethanol-induced locomotor activation, which have been linked in theory and may have mechanisms in common. The appetitive effects of ethanol are significantly modulated by μ and δ opioid receptors, whereas μ but not δ receptors are involved in the motor stimulant effec...

  18. IL-6-deficient Mice Are Susceptible to Ethanol-induced Hepatic Steatosis: IL-6 Protects against Ethanol-induced Oxidative Stress and Mitochondrial Permeability Transition in the Liver

    OsamaEl-Assal; FengHong; Won-HoKim; SvetlanaRadaeva; BinGao

    2004-01-01

    Interleukin-6 (IL-6)-deficient mice are prone to ethanol-induced apoptosis and steatosis in the liver; however,the underlying mechanism is not fully understood. Mitochondrial dysfunction caused by oxidative stress is an early event that plays an important role in the pathogenesis of alcoholic liver disease. Therefore, we hypothesize that the protective role of IL-6 in ethanol-induced liver injury is mediated via suppression of ethanol-induced oxidative stress and mitochondrial dysfunction. To test this hypothesis, we examined the effects of IL-6 on ethanol-induced oxidative stress, mitochondrial injury, and energy depletion in the livers of IL-6 (-/-) mice and hepatocytes from ethanol-fed rats. Ethanol consumption leads to stronger induction of malondialdehyde (MDA) in IL-6 (-/-) mice compared to wild-type control mice, which can be corrected by administration of IL-6. In vitro,IL-6 treatment prevents ethanol-mediated induction of reactive oxygen species (ROS), MDA, mitochondrial permeability transition (MPT), and ethanol-mediated depletion of adenosine triphosphate (ATP) in hepatocytes from ethanol-fed rats. Administration of IL-6 in vivo also reverses ethanol-induced MDA and ATP depletion in hepatocytes. Finally, IL-6 treatment induces metallothionein protein expression, but not superoxide dismutase and glutathione peroxidase in cultured hepatocytes. In conclusion, IL-6 protects against ethanol-induced oxidative stress and mitochondrial dysfunction in hepatocytes v/a induction of metallothionein protein expression, which mav account for the nrotective role of IL-6 in alcoholic liver disease.

  19. IL-6-deficient Mice Are Susceptible to Ethanol-induced Hepatic Steatosis: IL-6 Protects against Ethanol-induced Oxidative Stress and Mitochondrial Permeability Transition in the Liver

    Osama El-Assal; Feng Hong; Won-Ho Kim; Svetlana Radaeva; Bin Gao

    2004-01-01

    Interleukin-6 (IL-6)-deficient mice are prone to ethanol-induced apoptosis and steatosis in the liver; however, the underlying mechanism is not fully understood. Mitochondrial dysfunction caused by oxidative stress is an early event that plays an important role in the pathogenesis of alcoholic liver disease. Therefore, we hypothesize that the protective role of IL-6 in ethanol-induced liver injury is mediated via suppression of ethanol-induced oxidative stress and mitochondrial dysfunction. To test this hypothesis, we examined the effects of IL-6 on ethanol-induced oxidative stress, mitochondrial injury, and energy depletion in the livers of IL-6 (-/-) mice and hepatocytes from ethanol-fed rats. Ethanol consumption leads to stronger induction of malondialdehyde (MDA) in IL-6 (-/-) mice compared to wild-type control mice, which can be corrected by administration of IL-6. In vitro,IL-6 treatment prevents ethanol-mediated induction of reactive oxygen species (ROS), MDA, mitochondrial permeability transition (MPT), and ethanol-mediated depletion of adenosine triphosphate (ATP) in hepatocytes from ethanol-fed rats. Administration of IL-6 in vivo also reverses ethanol-induced MDA and ATP depletion in hepatocytes. Finally, IL-6 treatment induces metallothionein protein expression, but not superoxide dismutase and glutathione peroxidase in cultured hepatocytes. In conclusion, IL-6 protects against ethanol-induced oxidative stress and mitochondrial dysfunction in hepatocytes via induction of metallothionein protein expression, which may account for the protective role of IL-6 in alcoholic liver disease.

  20. Peculiarities of accentuation of hightened speech responsibility profession representatives

    Корнєлаєва, Є. В.

    2015-01-01

    The article deals with the peculiarities of accentuation in the speech of politicians, actors, lecturers. Profession is one of the main components of the speaker's social status. Accentuation helps to reveal components of text which can be the communicative centre of the utterance. In this study an attempt is undertaken to describe the prosodic features of speech of the representatives of the professions with high voice responsibility in an extralinguistic situation without involving the dire...

  1. Involvement of seven in absentia homolog-1 in ethanol-induced apoptosis in neural crest cells

    Sun, Haijing; Chen, Xiaopan; Yuan, Fuqiang; Liu, Jie; Zhao, Yingming; Chen, Shao-yu

    2014-01-01

    Ethanol-induced apoptosis in selected cell populations is a major component of pathogenesis underlying ethanol-induced teratogenesis. However, there is a fundamental gap in understanding how ethanol leads to apoptosis in embryos. In this study, we investigate the role of seven in absentia homolog-1 (Siah1) protein, an E3 ubiquitin ligase, in ethanol-induced apoptosis. Using an in vitro model of neural crest cell (NCC), JoMa1.3 cells, we found that exposure to 100 mM ethanol resulted in a significant increase in Siah1 mRNA expression in NCCs, an ethanol-sensitive cell population implicated in Fetal Alcohol Spectrum Disorders (FASD). Treatment with 100 mM ethanol for 24 hours also significantly increased the protein expression of Siah1 in JoMa1.3 cells. The nuclear translocation and accumulation of Siah1 was evidenced in the cells exposed to ethanol. In addition, we have found that the inhibition of Siah1 function with siRNA prevents ethanol-induced increase in Siah1 protein expression and nuclear translocation in NCCs. Down-regulation of Siah1 by siRNA also greatly diminished ethanol-induced cell death and caspase-3 activation, indicating that inhibition of Siah1 can attenuate ethanol-induced apoptosis. These results strongly suggest that Siah1 plays an important role in ethanol-induced apoptosis in NCCs. PMID:25193017

  2. Deletion of circadian gene Per1 alleviates acute ethanol-induced hepatotoxicity in mice

    The severity of ethanol-induced liver injury is associated with oxidative stress and lipid accumulation in the liver. Core circadian clock is known to mediate antioxidative enzyme activity and lipid metabolism. However, the link between circadian clock and ethanol-induced hepatotoxicity remains unclear. Here we showed that extents of acute ethanol-induced liver injury and steatosis in mice exhibit circadian variations consistent with hepatic expression of Period (Per) genes. Mice lacking clock gene Per1 displayed less susceptible to ethanol-induced liver injury, as evidenced by lower serum transaminase activity and less severe histopathological changes. Ethanol-induced lipid peroxidation was alleviated in Per1−/− mice. However, Per1 deletion had no effect on antioxidants depletion caused by ethanol administration. Ethanol-induced triglycerides (TG) accumulation in the serum and liver was significantly decreased in Per1−/− mice compared with that in wild-type (WT) mice. Analysis of gene expression in the liver revealed peroxisome proliferators activated receptor-gamma (PPARγ) and its target genes related to TG synthesis are remarkably down-regulated in Per1−/− mice. HepG2 cells were treated with ethanol at 150 mM for 3 days. Per1 overexpression augmented lipid accumulation after treatment with ethanol in HepG2 cells, but had no effect on ethanol-induced oxidative stress. Expression of genes related to lipogenesis, including PPARγ and its target genes, was up-regulated in cells overexpressing Per1. In conclusion, these results indicated that circadian rhythms of ethanol-induced hepatotoxicity are controlled by clock gene Per1, and deletion of Per1 protected mice from ethanol-induced liver injury by decreasing hepatic lipid accumulation

  3. Low brain histamine content affects ethanol-induced motor impairment.

    Lintunen, Minnamaija; Raatesalmi, Kristiina; Sallmen, Tina; Anichtchik, Oleg; Karlstedt, Kaj; Kaslin, Jan; Kiianmaa, Kalervo; Korpi, Esa R; Panula, Pertti

    2002-02-01

    The effect of ethanol on motor performance in humans is well established but how neural mechanisms are affected by ethanol action remains largely unknown. To investigate whether the brain histaminergic system is important in it, we used a genetic model consisting of rat lines selectively outbred for differential ethanol sensitivity. Ethanol-sensitive rats had lower levels of brain histamine and lower densities of histamine-immunoreactive fibers than ethanol-insensitive rats, although both rat lines showed no changes in histamine synthesizing neurons. Lowering the high brain histamine content of the ethanol-insensitive rats with alpha-fluoromethylhistidine before ethanol administration increased their ethanol sensitivity in a behavioral motor function test. Higher H3 receptor ligand binding and histamine-induced G-protein activation was detected in several brain regions of ethanol-naive ethanol-sensitive rats. Brain histamine levels and possibly signaling via H3 receptors may thus correlate with genetic differences in ethanol-induced motor impairment. PMID:11848689

  4. Sphingosine-1 phosphate prevents ethanol-induced corneal epithelial apoptosis

    Pierre Fournie

    2012-01-01

    Full Text Available Background: Apoptosis is a programmed cell death in multicellular organisms, found in a wide variety of conditions, including inflammatory process, everywhere in the body, including the cornea and conjunctiva. Aim: To evaluate the effect of a new topical formulation of sphingosine-1 phosphate on preventing apoptosis of the corneal epithelium. Setting: Medical University. Materials and Methods: We tested several formulations suitable for topical application. Twenty-five rabbits were distributed among five groups. Group 1 comprised the controls. In Group 2, 20% ethanol was applied topically for 20 seconds; in Group 3, 50 μM topical sphingosine-1 phosphate was applied 2 hours prior to 20% ethanol application. In Group 4, 200 μM topical sphingosine-1 phosphate was applied 2 hours before the 20% ethanol application. In Group 5, only 200 μM topical sphingosine-1 phosphate was applied. Apoptosis was evaluated using the terminal deoxynucleotidyl transferase biotin-dUTP Nick End Labeling (TUNEL assay. Pairwise comparisons were performed using t-tests with Scheffe′s correction. Data were analyzed using STATA 9.0 statistical software. Results: A suspension of sphingosine-1 phosphate in the presence of Montanox 80 was stable and could be formulated without sonication. Epithelial apoptosis was detected only in Groups 2 and 3. Conclusion: Sphingosine-1 phosphate can prevent ethanol-induced apoptosis in the corneal epithelium of rabbits.

  5. Glycine inhibits ethanol-induced oxidative stress, neuroinflammation and apoptotic neurodegeneration in postnatal rat brain.

    Amin, Faiz Ul; Shah, Shahid Ali; Kim, Myeong Ok

    2016-06-01

    Here we investigated for the first time the inhibitory potential of Glycine (Gly) against ethanol-induced oxidative stress, neuroinflammation and apoptotic neurodegeneration in human neuroblastoma SH-SY5Y cells and in the developing rat brain. The Gly co-treatment significantly increased the cell viability, inhibited the expression of phospho-Nuclear Factor kappa B (p-NF-kB) and caspase-3 and reduced the oxidative stress in ethanol-treated SH-SY5Y cells in a PI3K-dependent manner. Seven days old male rat pups were injected with ethanol (5 g/kg subcutaneously, prepared in a 20% saline solution) and Gly (1 g/kg). Gly co-treatment stimulated the PI3K/Akt signaling pathway to limit the ethanol induced reactive oxygen species (ROS) production in the developing rat brain. It lowered the ethanol-elevated levels of phospho-c Jun N terminal kinase (p-JNK) and its various downstream apoptotic markers, including Bax, cytochrome C, caspase-3 and PARP-1. Additionally, the Gly treatment upregulated antiapoptotic Bcl-2 proteins and prevented ethanol-induced neurodegeneration as assessed by Fluoro-Jade-B (FJB) and Nissl staining. Furthermore, the Gly administration caused significant reduction in the ethanol-induced neuroinflammation by inhibiting the expression of inflammatory markers such as p-NF-kB, cyclooxygenase 2 (COX2) and tumor necrosis factor-α (TNF-α) and reversed the ethanol-induced synaptic protein markers expression. The results suggest that acute Gly treatment reduces ethanol-induced oxidative stress and neuronal cell loss in SH-SY5Y cells and in the developing rat brain. Therefore, Gly may be considered as potential treatment in ethanol-intoxicated newborns and infants. PMID:27058626

  6. Early maternal separation affects ethanol-induced conditioning in a nor-BNI insensitive manner, but does not alter ethanol-induced locomotor activity.

    Pautassi, Ricardo Marcos; Nizhnikov, Michael E; Fabio, Ma Carolina; Spear, Norman E

    2012-01-01

    Early environmental stress significantly affects the development of offspring. This stress has been modeled in rats through the maternal separation (MS) paradigm, which alters the functioning of the HPA axis and can enhance ethanol intake at adulthood. Infant rats are sensitive to ethanol's reinforcing effects, which modulate ethanol seeking and intake. Little is known about the impact of MS on sensitivity to ethanol's appetitive and aversive effects during infancy. The present study assessed ethanol-induced conditioned place preference established through second-order conditioning (SOC), spontaneous or ethanol-induced locomotor activity and ethanol intake in preweanling rats that experienced normal animal facility rearing (AFR) or daily episodes of maternal separation (MS) during postnatal days 1-13 (PDs 1-13). Low-ethanol dose (0.5 g/kg) induced appetitive conditioned place preference (via SOC) in control rats given conventional rearing but not in rats given maternal separation in early infancy, whereas 2.0 g/kg ethanol induced aversive conditioned place preference in the former but not the latter. The administration of a kappa antagonist at PD 1 or immediately before testing did not alter ethanol-induced reinforcement. High (i.e., 2.5 and 2.0 g/kg) but not low (i.e., 0.5 g/kg) ethanol dose induced reliable motor stimulation, which was independent of early maternal separation. Ethanol intake and blood alcohol levels during conditioning were unaffected by rearing conditions. Pups given early maternal separation had lower body weights than controls and showed an altered pattern of exploration when placed in an open field. These results indicate that, when assessed in infant rats, earlier maternal separation alters the balance between the appetitive and aversive motivational effects of ethanol but has no effect on the motor activating effects of the drug. PMID:22108648

  7. EFFECT OF VIMLIV ON LIPID PEROXIDES AND ANTIOXIDANTS IN ETHANOL INDUCED HEPATOTOXICITY IN ALBINO WISTER RATS

    M. Samundeeswari and M. Rajadurai*

    2012-01-01

    This study was carried out to investigate the hepatoprotective and antioxidant properties of vimliv in ethanol-induced hepatotoxicity in rats. The liver toxicity was induced by the administration of ethanol to the animals at dose of 3 g/kg orally for 35 days. During the period of vimliv was co-administered to the rats at doses of 25 and 50 mg/kg for 35 days. The levels of lipidperoxidative products significantly increased and the levels of antioxidants decreased in ethanol induced rats. Co-ad...

  8. [Diagnosis of an organic disease in an accentuated personality].

    Rösner, K; Bretzke, G

    1979-12-01

    In a female patient with Dunbar-syndrome the cause of the complaints is not recognized during 18 years. Therefore, the symptomatology of the stenosis of the truncus coeliacus is briefly outlined. The patient reacts more and more neurotic on the misunderstanding of organically conditioned complaints, so that at last a consilium of experienced specialists makes the diagnosis "functional intestinal disturbances, hypchondriac depressive syndrome in accentuated personality". Therefore functional disturbances are to be diagnosed only then (also in the psychopathologic behaviour of the patients!), when an organic disease is excluded. The difficulty to justify such a demand is great. PMID:550625

  9. Curcuma aromatica Water Extract Attenuates Ethanol-Induced Gastritis via Enhancement of Antioxidant Status

    Woo-Young Jeon

    2015-01-01

    Full Text Available Curcuma aromatica is an herbal medicine and traditionally used for the treatment of various diseases in Asia. We investigated the effects of C. aromatica water extract (CAW in the stomach of rats with ethanol-induced gastritis. Gastritis was induced in rats by intragastric administration of 5 mL/kg body weight of absolute ethanol. The CAW groups were given 250 or 500 mg of extract/kg 2 h before administration of ethanol, respectively. To determine the antioxidant effects of CAW, we determined the level of lipid peroxidation, the level of reduced glutathione (GSH, the activities of catalase, degree of inflammation, and mucus production in the stomach. CAW reduced ethanol-induced inflammation and loss of epithelial cells and increased the mucus production in the stomach. CAW reduced the increase in lipid peroxidation associated with ethanol-induced gastritis (250 and 500 mg/kg, p<0.01, resp. and increased mucosal GSH content (500 mg/kg, p<0.01 and the activity of catalase (250 and 500 mg/kg, p<0.01, resp.. CAW increased the production of prostaglandin E2. These findings suggest that CAW protects against ethanol-induced gastric mucosa injury by increasing antioxidant status. We suggest that CAW could be developed for the treatment of gastritis induced by alcohol.

  10. Protective effect of tetrahydrocoptisine against ethanol-induced gastric ulcer in mice

    Excessive alcohol consumption can lead to gastric ulcer and the present work was aimed to examine the protective effect of tetrahydrocoptisine (THC) in the model of ethanol-induced gastric ulcer in mice. Fasted mice treated with ethanol 75% (0.5 ml/100 g) were pre-treated with THC (10 or 20 mg/kg, ip), cimetidine (100 mg/kg, ip) or saline in different experimental sets for a period of 3 days, and animals were euthanized 4 h after ethanol ingestion. Gross and microscopic lesions, immunological and biochemical parameters were taken into consideration. The results showed that ethanol induced gastric damage, improving nitric oxide (NO) level, increased pro-inflammatory cytokine (TNF-α and IL-6) levels and myeloperoxidase (MPO) activity, as well as the expression of nuclear factor-κB (NF-κB) in the ethanol group. Pretreatment of THC at doses of 10 and 20 mg/kg bodyweight significantly attenuated the gastric lesions as compared to the ethanol group. These results suggest that the gastroprotective activity of THC is attributed to reducing NO production and adjusting the pro-inflammatory cytokine, inhibited neutrophil accumulation and NF-κB expression. - Highlights: • THC decreased ethanol-induced pro-inflammatory cytokine release. • THC inhibited the production of NO in serum and gastric tissue. • THC reduced NF-κB expression and MPO accumulation in ethanol-induced gastric tissue

  11. Zinc inhibits ethanol-induced HepG2 cell apoptosis

    Alcohol consumption produces a variety of metabolic alterations in liver cells, associated with ethanol oxidation and with nonoxidative metabolism of ethanol, among others apoptosis of hepatocytes. As zinc is known as a potent antioxidant and an inhibitor of cell apoptosis, the aim of this paper was to investigate whether zinc supplementation could inhibit ethanol-induced HepG2 apoptosis, and whether this inhibition was connected with attenuation of oxidative stress and modulation of FasR/FasL system expression. The results indicated that zinc supplementation significantly inhibited ethanol-induced HepG2 cell apoptosis (measured by cytochrome c release from mitochondria and caspase-3 activation) by attenuation of reactive oxygen species (ROS) production, increase in the cellular level of GSH, inhibition of ethanol-induced sFasR and FasL overexpression and caspase-8 activation. These results indicate that zinc can inhibit ethanol-induced hepatocyte apoptosis by several independent mechanisms, among others by an indirect antioxidative effect and probably by inhibition of caspase-8 and caspase-9 activation

  12. The Future of Qualitative Research in Psychology: Accentuating the Positive.

    Gough, Brendan; Lyons, Antonia

    2016-06-01

    In this paper we reflect on current trends and anticipate future prospects regarding qualitative research in Psychology. We highlight various institutional and disciplinary obstacles to qualitative research diversity, complexity and quality. At the same time, we note some causes for optimism, including publication breakthroughs and vitality within the field. The paper is structured into three main sections which consider: 1) the positioning of qualitative research within Psychology; 2) celebrating the different kinds of knowledge produced by qualitative research; and 3) implementing high quality qualitative research. In general we accentuate the positive, recognising and illustrating innovative qualitative research practices which generate new insights and propel the field forward. We conclude by emphasising the importance of research training: for qualitative research to flourish within Psychology (and beyond), students and early career researchers require more sophisticated, in-depth instruction than is currently offered. PMID:26179872

  13. PRENATAL ETHANOL EXPOSURE LEADS TO GREATER ETHANOL-INDUCED APPETITIVE REINFORCEMENT

    Ricardo M. Pautassi; Nizhnikov, Michael E.; Norman E. Spear; Molina, Juan C.

    2012-01-01

    Prenatal ethanol significantly heightens later alcohol consumption, but the mechanisms that underlie this phenomenon are poorly understood. Little is known about the basis of this effect of prenatal ethanol on the sensitivity to ethanol’s reinforcing effects. One possibility is that prenatal ethanol exposure makes subjects more sensitive to the appetitive effects of ethanol or less sensitive to ethanol’s aversive consequences. The present study assessed ethanol-induced second-order conditione...

  14. Hepatoprotective effect of Piper guineense aqueous extract against ethanol-induced toxicity in male rats

    Babatunji E. Oyinloye; Adeyinka A. Ajagbe; Sarah O. Nwozo

    2012-01-01

    Objective: Herbal medicinal products play an important role in the management of liver diseases for the lack of satisfactory liver protective drugs in allopathic medical practices. Searching for hepatoprotective drugs with high efficacy and safety is of great need. Our aim is to evaluate the hepatoprotective and antioxidant effect of aqueous extract of Piper guineense (P.G.) on ethanol induced toxicity in Wistar rats. Methods: In order to assess the hepatoprotective effect of this extract in ...

  15. Study of antioxidant potential of malotilate in ethanol induced hepatic dysfunction in Sprague Dawley rats

    Kanchan Dnyanesh Borole; Ravi Swami; Pradnya Hemant Padalkar

    2016-01-01

    Background: Alcoholic liver disease (ALD) is one of the major causes of mortality and morbidity worldwide. Objective of the study was to elicit a preventive mechanism of malotilate, a reported potent hepatoprotective agent, against ethanol induced sub-acute hepatotoxicity. Both ethanol and malotilate were administered for 21 days to evaluate the toxicity and prevention by the drug molecule. Methods: Thirty adult healthy Sprague Dawley rats of either sex, weighing 200-250 g selected for the...

  16. Evaluation of Spirulina Supplementation on Intermittent Binge Ethanol - Induced Neurotoxicity in Dentate Gyrus of Rats

    M A Asari

    2013-03-01

    Full Text Available Summary. Spirulina is a widely used nutritional supplement which is rich in antioxidants and proteins.  Studies have shown that intermittent binge-like ethanol consumption during adolescent period caused neuronal damage in specific parts of the brain, including the dentate gyrus. It has been suggested that antioxidant therapy may provide some level of protection against neurotoxicity of ethanol at cellular level. Therefore, the purpose of this study was to examine the preventive effects of spirulina supplementation on ethanol-induced neurotoxicity in the dentate gyrus of adolescent rats. Male Sprague-Dawley rats were given ethanol (10 g/kg/day, intermittent binge model, or spirulina platensis (1000 mg/kg/day or both from postnatal day 30 for two weeks duration. The cerebral hemispheres were processed for routine histological staining and immunohistochemistry with anti-GFAP antibody.  Ethanol-treated group showed significant deficit in the numbers of granule cells and hilar neurons of the dentate gyrus when compared to the control group. Spirulina supplementation failed to provide protection against ethanol-induced neuronal loss. Spirulina supplementation also failed to alter increased expression of GFAP immunoreactivity induced by ethanol exposure. In conclusion, these findings indicate that spirulina supplementation is not effective in reducing the ethanol-induced neurotoxicity in the dentate gyrus of adolescent rats. Industrial Relevance. Spirulina is one of the widely used nutritional supplements particularly in Asian population. Being a strong antioxidant, spirulina has been shown to have many therapeutic effects in human. However, the question of whether spirulina supplementation is able to mitigate the effect of ethanol neurotoxicity is largely unknown. Therefore, the study was undertaken to investigate the possibility that spirulina supplementation is able to provide some protection against ethanol-induced neurotoxicity in a rat model

  17. Protective effects of Ginkgo biloba extract on the ethanol-induced gastric ulcer in rats

    Sheng-Hsuan Chen; Yu-Chih Liang; Jane CJ Chao; Li-Hsueh Tsai; Chun-Chao Chang; Chia-Chi Wang; Shiann Pan

    2005-01-01

    AIM: To evaluate the preventive effect of Ginkgo bilobaextract (GbE) on ethanol-induced gastric mucosal injuries in rats.METHODS: Female Wistar albino rats were used for the studies. We randomly divided the rats for each study into five subgroups: normal control, experimental control, and three experimental groups. The gastric ulcers were induced by instilling 1 mL 50% ethanol into the stomach. We gaveGbE 8.75, 17.5, 26.25 mg/kg intravenously to the experimental groups respectively 30 min prior to the ulcerative challenge. We removed the stomachs 45 min later. The gastric ulcers,gastric mucus and the content of non-protein sulfhydryl groups (NP-SH), malondialdehyde (MDA), c-Jun kinase (JNK) activity in gastric mucosa were evaluated. The amount of gastric juice and its acidity were also measured. RESULTS: The findings of our study are as follows: (1)GbE pretreatment was found to provide a dose-dependent protection against the ethanol-induced gastric ulcers in rats; (2) the GbE pretreatment afforded a dose-dependent inhibition of ethanol-induced depletion of stomach wall mucus, NP-SH oontents and increase in the lipid peroxidation (increase MDA) in gastric tissue; (3) gastric ulcer induced by ethanolproduced an increase in JNK activity in gastric mucosawhich also significantly inhibited by pretreatment with GbE;and (4) GbE alone had no inhibitory effect on gastric secretionin pylorus-ligated rats.CONCLUSION: The finding of this study showed that GbE significantly inhibited the ethanol-induced gastric lesions in rats. We suggest that the preventive effect of GbE may be mediated through: (1) inhibition of lipid peroxidation;(2) preservation of gastric mucus and NP-SH; and (3)blockade of cell apoptosis.

  18. Oxidative stress disturbs energy metabolism of mitochondria in ethanol-induced gastric mucosa injury

    Jin-Shui Pan, Shao-Zhen He, Hong-Zhi Xu, Xiao-Juan Zhan, Xiao-Ning Yang, Hong-Min Xiao, Hua-Xiu Shi, Jian-Lin Ren

    2008-10-01

    Full Text Available AIM: To study the role of mitochondrial energy disorder in the pathogenesis of ethanol-induced gastric mucosa injury.METHODS: Wistar rats were used in this study. A gastric mucosal injury model was established by giving the rats alcohol. Gross and microscopic appearance of gastric mucosa and ultrastructure of mitochondria were evaluated. Malondiadehyde (MDA in gastric mucosa was measured with thiobarbituric acid. Expression of ATP synthase (ATPase subunits 6 and 8 in mitochondrial DNA (mtDNA was determined by reverse transcription polymerase chain reaction (RT-PCR.RESULTS: The gastric mucosal lesion index was correlated with the MDA content in gastric mucosa. As the concentration of ethanol was elevated and the exposure time to ethanol was extended, the content of MDA in gastric mucosa increased and the extent of damage aggravated. The ultrastructure of mitochondria was positively related to the ethanol concentration and exposure time. The expression of mtDNA ATPase subunits 6 and 8 mRNA declined with the increasing MDA content in gastric mucosa after gavage with ethanol.CONCLUSION: Ethanol-induced gastric mucosa injury is related to oxidative stress, which disturbs energy metabolism of mitochondria and plays a critical role in the pathogenesis of ethanol-induced gastric mucosa injury.

  19. Ethanol-induced loss of brain cyclic AMP binding proteins: correlation with growth suppression

    Brain hypoplasia secondary to maternal ethanol consumption is a common fetal defect observed in all models of fetal alcohol syndrome. The molecular mechanism by which ethanol inhibits growth is unknown but has been hypothesized to involve ethanol-induced changes in the activity of cyclic-AMP stimulated protein kinase. Acute and chronic alcohol exposure elevate cyclic AMP level in many tissues, including brain. This increase in cyclic AMP should increase the phosphorylating activity of kinase by increasing the amount of dissociated (active) kinase catalytic subunit. In 7-day embryonic chick brains, ethanol-induced growth suppression was correlated with increased brain cyclic AMP content but neither basal nor cyclic AMP stimulated kinase catalytic activity was increased. However, the levels of cyclic AMP binding protein (kinase regulatory subunit) were significantly lowered by ethanol exposure. Measured as either 3H cyclic AMP binding or as 8-azido cyclic AM32P labeling, ethanol-exposed brains had significantly less cyclic AMP binding activity (51 +/- 14 versus 29 +/- 10 units/μg protein for 8-azido cyclic AMP binding). These findings suggest that ethanol's effect on kinase activity may involve more than ethanol-induced activation of adenylate cyclase

  20. Antioxidative Activity of Flavonoids from Abrus cantoniensis against Ethanol-Induced Gastric Ulcer in Mice.

    Li, Hui; Song, Zi-Jing; Dai, Yan-Ping; Zhang, Su-Li; He, Xin; Guo, Chang-Run; Zhang, Wen-Jun; Wang, Jiao-Ying; Zhang, Chun-Feng; Wang, Chong-Zhi; Yuan, Chun-Su

    2015-07-01

    The present study investigated the flavonoids from Abrus cantoniensis against ethanol-induced gastric ulcers in mice. The flavonoids from A. cantoniensis were extracted with ethanol and purified by macroporous resin and polyamide. The 2,2-diphenyl-1-picrylhydrazyl assay was used to measure the antioxidative activities in vitro. The ethanol-induced ulcer mouse model was used to evaluate the gastroprotective activities of the flavonoids from A. cantoniensis. In addition, a method was established to ensure accuracy for animal ulcer evaluation. The flavonoids from A. cantoniensis showed a strong free radical scavenging capacity with an IC50 of 43.83 µg/mL in the 2,2-diphenyl-1-picrylhydrazyl assay. At doses between 28.16-112.67 mg/kg, the flavonoids conspicuously reduced the ulcer index in ethanol-induced mice (pdefensive mechanism. The data revealed that the flavonoids from A. cantoniensis could be a potential therapeutic agent for gastric ulcer prevention and treatment. PMID:26039267

  1. Protective effect of vitamin E against ethanol-induced small intestine damage in rats.

    Shirpoor, Alireza; Barmaki, Hanieh; Khadem Ansari, Mohamadhasan; Lkhanizadeh, BehrouzI; Barmaki, Haleh

    2016-03-01

    The role of oxidative stress and inflammatory reaction has been reported in various ethanol-induced complications. The purpose of this study was to evaluate the effect of ethanol-induced structural alteration, oxidative stress, and inflammatory reaction on the small intestine of rats, and plausible protective effect of vitamin E to determine whether it inhibits the abnormality induced by ethanol in the small intestine. Twenty-four male wistar rats were divided into three groups, namely: Control(©), ethanol, and vitamin E treated ethanol groups. After six weeks of treatment, the small intestine length, villus height, crypt depth and muscular layer thickness, oxidative stress, and inflammatory parameters showed significant changes in the ethanol treated group compared to the control group. Vitamin E consumption along with ethanol ameliorated structural alteration of the small intestine and reduced the elevated amount of oxidative stress and inflammatory markers such as protein carbonyl, OX-LDL, IL-6, Hcy, and TNF-α. Furthermore, their total antioxidant capacity was increased significantly compared to that of the ethanol group. These findings indicate that ethanol induces the small intestine abnormality by oxidative and inflammatory stress, and that these effects can be alleviated by using vitamin E as an antioxidant and anti-inflammatory molecule. PMID:26898436

  2. Tetrahydroxystilbene glucoside protects against ethanol-induced liver injury in mice by inhibition of expression of inflammatuion-related factors

    熊章鄂

    2013-01-01

    Objective To investigate the protective effects of tetrahydroxystilbene glucoside(TSG)against acute ethanol-induced liver injury in mice and to explore the possible mechanisms involved.Methods Kunming mice were

  3. Salvia miltiorrhiza Bunge Blocks Ethanol-Induced Synaptic Dysfunction through Regulation of NMDA Receptor-Dependent Synaptic Transmission

    Park, Hye Jin; Lee, Seungheon; Jung, Ji Wook; Lee, Young Choon; Choi, Seong-Min; Kim, Dong hyun

    2016-01-01

    Consumption of high doses of ethanol can lead to amnesia, which often manifests as a blackout. These blackouts experienced by ethanol consumers may be a major cause of the social problems associated with excess ethanol consumption. However, there is currently no established treatment for preventing these ethanol-induced blackouts. In this study, we tested the ethanol extract of the roots of Salvia miltiorrhiza (SM) for its ability to mitigate ethanol-induced behavioral and synaptic deficits. ...

  4. Antioxidant and antiulcer potential of aqueous leaf extract of Kigelia africana against ethanol-induced ulcer in rats

    dos Santos, Matheus M; Olaleye, Mary T.; Ineu, Rafael P.; Aline A. Boligon; Margareth L. Athayde; Barbosa, Nilda B.V.; Rocha, João B. T.

    2014-01-01

    Ethnobotanical claims regarding Kigelia africana reported antiulcer properties as part of its medicinal application. In this work, aqueous leaf extract from K. africana was investigated for its phytochemical constituents and antiulcer potential against ethanol-induced ulcer in rats. The participation of oxidative stress on ethanol-induced ulcer and the potential protective antioxidant activity of K. africana extracts were investigated by determining vitamin C and thiobarbituric acid reactive ...

  5. Influence of zinc sulfate intake on acute ethanol-induced liver injury in rats

    Sema Bolkent; Pelin Arda-Pirincci; Sehnaz Bolkent; Refiye Yanardag; Sevim Tunali; Sukriye Yildirim

    2006-01-01

    AIM: To investigate the role of metallothionein and proliferating cell nuclear antigen (PCNA) on the morphological and biochemical effects of zinc sulfate in ethanol-induced liver injury.METHODS: Wistar albino rats were divided into four groups. Group I; intact rats, group Ⅱ; control rats given only zinc, group Ⅲ; animals given absolute ethanol, group Ⅳ; rats given zinc and absolute ethanol.Ethanol-induced injury was produced by the 1 mL of absolute ethanol, administrated by gavage technique to each rat. Animals received 100 mg/kg per day zinc sulfate for 3 d 2 h prior to the administration of absolute ethanol.RESULTS: Increases in metallothionein immunoreactivity in control rats given only zinc and rats given zinc and ethanol were observed. PCNA immunohistochemistry showed that the number of PCNA-positive hepatocytes was increased significantly in the livers of rats administered ethanol + zinc sulfate. Acute ethanol exposure caused degenerative morphological changes in the liver. Blood glutathione levels decreased, serum alkaline phosphatase and aspartate transaminase activities increased in the ethanol group when compared to the control group. Liver glutathione levels were reduced, but lipid peroxidation increased in the livers of the group administered ethanol as compared to the other groups. Administration of zinc sulfate in the ethanol group caused a significant decrease in degenerative changes, lipid peroxidation, and alkaline phosphatase and aspartate transaminase activities, but an increase in liver glutathione.CONCLUSION: Zinc sulfate has a protective effect on ethanol-induced liver injury. In addition, cell proliferation may be related to the increase in metallothionein immunoreactivity in the livers of rats administered ethanol + zinc sulfate.

  6. Antioxidant Effect of Carica papaya on Ethanol Induced Gastric Lesion in Adult Male Wistar Rats

    A.A. Okesina

    2012-06-01

    Full Text Available This study was performed to elucidate the role of some important constituents of antioxidant defence such as Glutathione Peroxidase (GPx, Thiobarbituric Acid Reaction (TBAR, the activity of the enzyme Glucose-6-Phosphate Dehydrogenase (G-6-PDH of Carica papaya on ethanol induced gastric lesion in adult male wistar rats. Twenty-four male adult Wistar rats weighing 180- 220 g were used in this study. Animals were divided into three groups (n = 8 per group. The control group A received phosphate buffered saline orally, with the aid of a cannula. 1 mL of 50% ethanol was administered orally, by a cannula, to produce the gastric lesion in group B (n = 8. And in the group C, 500 mg/kg body weight of paw paw leaf extract was administered orally, with a cannula, twelve hours after ethanol administration to the rats. This experiment lasted for twenty one consecutive days. The result showed that TBARS in gastric mucosa as an index for oxidative stress level was significantly increased after ethanol administration. CPL did not reduce significantly the levels of TBARS in the gastric mucosa. G-6-PDH activity was significantly increased in gastric mucosa after ethanol administration, but in rats treated with CPL, a reverse of G-6-PDH activity was observed. Ethanol induced a remarkable and significant decrease of GPx activity in gastric mucosa, whereas CPL induced a significant reversion of ethanol’s effect on the enzyme. The results therefore demonstrate that CPL treatment exerts antioxidant effects on ethanol-induced gastric lesions in wistar rats.

  7. Autophagy Protects against CYP2E1/Chronic Ethanol-Induced Hepatotoxicity

    Yongke Lu

    2015-10-01

    Full Text Available Autophagy is an intracellular pathway by which lysosomes degrade and recycle long-lived proteins and cellular organelles. The effects of ethanol on autophagy are complex but recent studies have shown that autophagy serves a protective function against ethanol-induced liver injury. Autophagy was found to also be protective against CYP2E1-dependent toxicity in vitro in HepG2 cells which express CYP2E1 and in vivo in an acute alcohol/CYPE1-dependent liver injury model. The goal of the current report was to extend the previous in vitro and acute in vivo experiments to a chronic ethanol model to evaluate whether autophagy is also protective against CYP2E1-dependent liver injury in a chronic ethanol-fed mouse model. Wild type (WT, CYP2E1 knockout (KO or CYP2E1 humanized transgenic knockin (KI, mice were fed an ethanol liquid diet or control dextrose diet for four weeks. In the last week, some mice received either saline or 3-methyladenine (3-MA, an inhibitor of autophagy, or rapamycin, which stimulates autophagy. Inhibition of autophagy by 3-MA potentiated the ethanol-induced increases in serum transaminase and triglyceride levels in the WT and KI mice but not KO mice, while rapamycin prevented the ethanol liver injury. Treatment with 3-MA enhanced the ethanol-induced fat accumulation in WT mice and caused necrosis in the KI mice; little or no effect was found in the ethanol-fed KO mice or any of the dextrose-fed mice. 3-MA treatment further lowered the ethanol-decrease in hepatic GSH levels and further increased formation of TBARS in WT and KI mice, whereas rapamycin blunted these effects of ethanol. Neither 3-MA nor rapamycin treatment affected CYP2E1 catalytic activity or content or the induction CYP2E1 by ethanol. The 3-MA treatment decreased levels of Beclin-1 and Atg 7 but increased levels of p62 in the ethanol-fed WT and KI mice whereas rapamycin had the opposite effects, validating inhibition and stimulation of autophagy, respectively. These

  8. Camellia sinensis (L.) Kuntze Extract Ameliorates Chronic Ethanol-Induced Hepatotoxicity in Albino Rats

    Poonam Lodhi; Neeraj Tandan; Neera Singh; Divyansh Kumar; Monu Kumar

    2014-01-01

    The goal of this study was to investigate the hepatoprotective effects of aqueous extract of Camellia sinensis or green tea extract (AQGTE) in chronic ethanol-induced albino rats. All animals were divided into 4 groups in the study for a 5-week duration. 50% ethanol was given orally to the rats with two doses (5 mg/kg bw and 10 mg/kg bw) of AQGTE. Ethanol administration caused a significant increase in the levels of plasma and serum enzymatic markers, alanine aminotransferase (ALT), aspartate...

  9. Autophagy Protects against CYP2E1/Chronic Ethanol-Induced Hepatotoxicity

    Yongke Lu; Cederbaum, Arthur I.

    2015-01-01

    Autophagy is an intracellular pathway by which lysosomes degrade and recycle long-lived proteins and cellular organelles. The effects of ethanol on autophagy are complex but recent studies have shown that autophagy serves a protective function against ethanol-induced liver injury. Autophagy was found to also be protective against CYP2E1-dependent toxicity in vitro in HepG2 cells which express CYP2E1 and in vivo in an acute alcohol/CYPE1-dependent liver injury model. The goal of the current re...

  10. Neuroprotection by taurine in ethanol-induced apoptosis in the developing cerebellum

    Taranukhin Andrey G; Taranukhina Elena Y; Saransaari Pirjo; Podkletnova Irina M; Pelto-Huikko Markku; Oja Simo S

    2010-01-01

    Abstract Background Acute ethanol administration leads to massive apoptotic neurodegeneration in the developing central nervous system. We studied whether taurine is neuroprotective in ethanol-induced apoptosis in the mouse cerebellum during the postnatal period. Methods The mice were divided into three groups: ethanol-treated, ethanol+taurine-treated and controls. Ethanol (20% solution) was administered subcutaneously at a total dose of 5 g/kg (2.5 g/kg at time 1 h and 2.5 g/kg at 3 h) to th...

  11. Aphrodisiac Activity and Curative Effects of Pedalium Murex (L) Against Ethanol Induced Infertility in Male Rats

    BALAMURUGAN, Gunasekaran; P. Muralidharan; POLAPALA, Satyanarayana

    2010-01-01

    It has been suggested that chronic ethanol exposure may result in testicular damage and infertility in males. Petroleum ether extract of Pedalium murex, family Pedaliaceae (PEPM), is evaluated in this study for its ability to increase aphrodisiac activity and to cure ethanol induced germ cell damage and infertility in male rat models. Doses of 200 and 400 mg/kg of PEPM showed a significant increase (P < 0.01, P < 0.001) in mating and mounting behaviour. The effect on fertility factors s...

  12. Acquisition and reinstatement of ethanol-induced conditioned place preference in rats: Effects of the cholinesterase inhibitors donepezil and rivastigmine.

    Gawel, Kinga; Labuz, Krzysztof; Gibula-Bruzda, Ewa; Jenda, Malgorzata; Marszalek-Grabska, Marta; Silberring, Jerzy; Kotlinska, Jolanta H

    2016-07-01

    The present study examined the influence of the cholinesterase inhibitors donepezil (a selective inhibitor of acetylcholinesterase) and rivastigmine (also an inhibitor of butyrylcholinesterase) on the acquisition and reinstatement of ethanol-induced conditioned place preference (CPP) in rats. Before the CPP procedure, animals received a single injection of ethanol (0.5 g/kg, 10% w/v, intraperitoneally [i.p.]) for 15 days. The ethanol-induced CPP (biased method) was developed by four injections of ethanol (0.5 g/kg, 10% w/v, i.p.) every second day. Control rats received saline instead of ethanol. Donepezil (0.5, 1 or 3 mg/kg, i.p.) or rivastigmine (0.03, 0.5 or 1 mg/kg, i.p.) were administered before ethanol during conditioning or before the reinstatement of ethanol-induced CPP. The cholinesterase inhibitors were equally effective in increasing (dose dependently) the acquisition of ethanol-induced CPP. Furthermore, priming injections of both inhibitors reinstated (cross-reinstatement) the ethanol-induced CPP with similar efficacy. These effects of both cholinesterase inhibitors were reversed by mecamylamine (3 mg/kg, i.p.), a nicotinic acetylcholine receptor antagonist, but not by scopolamine (0.5 mg/kg, i.p.), a muscarinic acetylcholine receptor antagonist. Thus, our results show that the cholinergic system is involved in the reinforcing properties of ethanol, and nicotinic acetylcholine receptors play an important role in the relapse to ethanol-seeking behaviour. PMID:27097732

  13. Salvia miltiorrhiza Bunge Blocks Ethanol-Induced Synaptic Dysfunction through Regulation of NMDA Receptor-Dependent Synaptic Transmission.

    Park, Hye Jin; Lee, Seungheon; Jung, Ji Wook; Lee, Young Choon; Choi, Seong-Min; Kim, Dong Hyun

    2016-07-01

    Consumption of high doses of ethanol can lead to amnesia, which often manifests as a blackout. These blackouts experienced by ethanol consumers may be a major cause of the social problems associated with excess ethanol consumption. However, there is currently no established treatment for preventing these ethanol-induced blackouts. In this study, we tested the ethanol extract of the roots of Salvia miltiorrhiza (SM) for its ability to mitigate ethanol-induced behavioral and synaptic deficits. To test behavioral deficits, an object recognition test was conducted in mouse. In this test, ethanol (1 g/kg, i.p.) impaired object recognition memory, but SM (200 mg/kg) prevented this impairment. To evaluate synaptic deficits, NMDA receptor-mediated excitatory postsynaptic potential (EPSP) and long-term potentiation (LTP) in the mouse hippocampal slices were tested, as they are known to be vulnerable to ethanol and are associated with ethanol-induced amnesia. SM (10 and 100 μg/ml) significantly ameliorated ethanol-induced long-term potentiation and NMDA receptor-mediated EPSP deficits in the hippocampal slices. Therefore, these results suggest that SM prevents ethanol-induced amnesia by protecting the hippocampus from NMDA receptor-mediated synaptic transmission and synaptic plasticity deficits induced by ethanol. PMID:27257009

  14. Nuclear effects of ethanol-induced proteasome inhibition in liver cells

    Fawzia Bardag-Gorce

    2009-01-01

    Alcohol ingestion causes alteration in several cellular mechanisms, and leads to inflammation, apoptosis,immunological response defects, and fibrosis. These phenomena are associated with significant changes in the epigenetic mechanisms, and subsequently,to liver cell memory. The ubiquitin-proteasome pathway is one of the vital pathways in the cell that becomes dysfunctionial as a result of chronic ethanol consumption. Inhibition of the proteasome activity in the nucleus causes changes in the turnover of transcriptional factors, histone modifying enzymes,and therefore, affects epigenetic mechanisms.Alcohol consumption has been associated with an increase in histone acetylation and a decrease in histone methylation, which leads to gene expression changes. DNA and histone modifications that result from ethanol-induced proteasome inhibition are key players in regulating gene expression, especially genes involved in the cell cycle, immunological responses,and metabolism of ethanol. The present review highlights the consequences of ethanol-induced proteasome inhibition in the nucleus of liver cells that are chronically exposed to ethanol.

  15. Polymer fraction of Aloe vera exhibits a protective activity on ethanol-induced gastric lesions.

    Park, Chul-Hong; Nam, Dong-Yoon; Son, Hyeong-U; Lee, Si-Rim; Lee, Hyun-Jin; Heo, Jin-Chul; Cha, Tae-Yang; Baek, Jin-Hong; Lee, Sang-Han

    2011-04-01

    For centuries, Aloe has been used as a herbal plant remedy against skin disorders, diabetes, and for its cardiac stimulatory activity. Here, we examined the gastroprotective effects of an Aloe vera polymer fraction (Avpf; molecular weight cut-off ≥50 kDa; 150 mg/kg body weight, p.o.) on an ethanol-induced gastric lesion mouse model. Mice pre-treated with Avpf had significantly fewer gastric lesions than their respective controls. To further examine the potential mechanism underlying this effect, we used reverse transcription-polymerase chain reaction to examine nitric oxide synthase and matrix metalloproteinase (MMP)mRNA expression on tissues from gastric lesions. Our results revealed that the mRNA expressions of inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS) were each reduced by ~50% in Avpf-treated mice vs. the controls, whereas, the mRNA expression levels of endothelial nitric oxide synthase remained unchanged. MMP-9, an index for gastric lesions, also alleviated the ethanol-treated gastric ulceration during Avpf treatment. These findings collectively suggest that Avpf significantly protects the gastric mucosa against ethanol-induced gastric damage, at least in part, by decreasing mRNA expression levels of not only iNOS and nNOS, but also MMP-9. PMID:21286662

  16. Protective role of intracellular glutathione against ethanol-induced damage in cultured rat gastric mucosal cells

    This study investigated whether intracellular glutathione is cytoprotective against ethanol-induced injury to cultured rat gastric mucosal cells in vitro. Secondly, it investigated whether reduced glutathione or oxidized glutathione is responsible for this cytoprotection. Cytolysis was quantified by measuring 51Cr release from prelabeled cells. Concentrations of ethanol greater than 12% caused cell damage and increased 51Cr release in a dose-dependent and time-related fashion. When a substrate for glutathione synthesis, N-acetyl-L-cysteine, was provided to cultured cells for 4 h before challenge with ethanol, cytolysis was significantly decreased corresponding with an increase in cellular glutathione content. Pretreatment with diethyl maleate, which depletes reduced glutathione without forming oxidized glutathione, potentiated ethanol-induced cell damage in a dose-dependent manner with the decrease of cellular glutathione content. The administration of tert-butyl hydroperoxide (which is specifically reduced by glutathione peroxidase to generate oxidized glutathione from reduced glutathione) or diamide (which nonenzymatically oxidizes reduced glutathione to oxidized glutathione) enhanced ethanol injury. We conclude that in cultured gastric mucosal cells, (a) intracellular glutathione maintains integrity of gastric mucosal cells against ethanol in vitro; and (b) reduced glutathione rather than oxidized glutathione is responsible for this cytoprotection. We postulate that the presence of reduced glutathione is essential to allow glutathione peroxidase to catalyze the ethanol-generated toxic oxygen radical, hydrogen peroxide

  17. Ethanol-induced impairment of hepatic glycoprotein secretion in the isolated rat liver perfusion model

    The authors have previously shown that acute administration of ethanol inhibits hepatic glycoprotein secretion in vivo. This ethanol-induced effect appears to be mediated by its reactive metabolite, acetaldehyde. Since hormonal influences and vascular changes can not be controlled in vivo during ethanol administration, they investigated the effect of ethanol in the isolated perfused liver model. Rat liver from fed animals was perfused with oxygenated KRB at 3 ml/min/g liver for 4 hrs. Since ethanol inhibits proteins synthesis in vitro, protein acceptor pool size was equalized in both ethanol and control perfused livers with 1 mM cycloheximide. 3H-glucosamine was used to label hepatic secretory glycoproteins in the perfusate. Colchicine, a known inhibitor of protein secretion, impaired the secretion of labeled glycoproteins with a concomitant retention of these export proteins in the liver; therefore, confirming the authors secretory model. Ethanol (50 mM) inhibited the appearance of glucosamine-labeled glycoproteins by 60% into the perfusate as compared to control livers. Pretreatment of animals with cyanamide (an aldehyde dehydrogenase inhibitor) further potentiated this effect of ethanol in the isolated perfused liver. These data suggest that ethanol inhibits hepatic glycoprotein secretion in the isolated liver perfusion model, and this ethanol-induced impairment appears to be mediated by acetaldehyde

  18. Ethanol-induced cell damage in cultured rat antral mucosa assessed by chromium-51 release

    We have developed an in vitro method for studying ethanol-induced injury to gastric mucosa using organ culture of rat antrum. Cell damage was assessed by measurement of the release of [51Cr]sodium chromate from preloaded cells, a method adapted from a standard immunologic technique. This system provided rapid and highly reproducible quantitation of tissue injury as assessed by 51Cr release into the culture medium. The threshold concentration for ethanol-induced damage was between 10 and 15% v/v, similar to in vivo thresholds observed by others. 51Cr release could also be induced by very short exposure to ethanol (5-15 min), and then continued despite ethanol removal. Interestingly, after continuous ethanol exposure, a plateau of maximum 51Cr release was reached 60 min after exposure to ethanol over the concentration range 20-50%, suggesting tissue adaptation to ethanol damage. This organ culture system, which allows precise control of experimental conditions, may be useful for studying mechanisms of gastric mucosal injury and protection

  19. Vitamin-C protect ethanol induced apoptotic neuro degeneration in postnatal rat brain

    Objective: To evaluate ethanol effects to induced activation of caspsae-3, and to observe the protective effects of Vitamin C (vit-C) on ethanol-induced apoptotic neuro degeneration in rat cortical area of brain. Methodology: Administration of a single dose of ethanol in 7-d postnatal (P7) rats triggers activation of caspase-3 and widespread apoptotic neuronal death. Western blot analysis, cells counting and Nissl staining were used to elucidate possible protective effect of vit-C against ethanol-induced apoptotic neuro degeneration in brain. Results: The results showed that ethanol significantly increased caspase-3 expression and neuronal apoptosis. Furthermore, the co-treatment of vit-C along with ethanol showed significantly decreased expression of caspase-3 as compare to control group. Conclusion: Our findings indicate that vit-C can prevent some of the deleterious effect of ethanol on developing rat brain when given after ethanol exposure and can be used as an effective protective agent for Fetal Alcohol Syndrome (FAS). (author)

  20. Structure and preventive effects against ethanol-induced gastric ulcer of an expolysaccharide from Lachnum sp.

    Xu, Ping; Yang, Liu; Yuan, Ru-Yue; Ye, Zi-Yang; Ye, Hui-Ran; Ye, Ming

    2016-05-01

    An extracellular polysaccharide of Lachnum sp. (LEP) was purified by DEAE-cellulose 52 column chromatography and Sepharose CL-6B column chromatography. LEP-2a was identified to be a homogeneous component with an average molecular weight of 3.22×10(4)Da. The structure of LEP-2a was characterized by chemical and spectroscopic methods, including methylation analysis, periodate oxidation-smith degradation, infrared spectroscopy and NMR analysis. Results indicated that LEP-2a was a (1→3)-,(1→6)-β-D-Glcp, whose branch chain was consist of two d-glucopyranosyl residues linked by β-1,3-glycosidic linkage, which was linked at C6 of the backbone chain by β-1,6-glycosidic linkage. To study the protective effects of LEP-2a on the ethanol-induced gastric ulcer in mice, LEP-2a (100, 200 and 400mg/kg/d) was given to mice by gavage for 2 weeks. Results showed that LEP-2a significantly decreased the ulcer bleeding areas, pepsin activity, gastric juice volume, gastric juice total acidity and the malondialdehyde (MDA) content in serum. Meanwhile, the superoxide dismutase (SOD) increased significantly. The above findings suggested that LEP-2a had a significant preventive effect against the ethanol-induced gastric ulcer. PMID:26774377

  1. Acetaminophen fails to inhibit ethanol-induced subjective effects in human volunteers.

    Pickworth, W B; Klein, S A; George, F R; Henningfield, J E

    1992-01-01

    In animals, ethanol causes some of its CNS effects by releasing prostaglandins (PG); this is demonstrated by reports that prostaglandin synthetase inhibitors (PGSIs) diminish ethanol-induced effects. However, use of animals in these studies has precluded testing for subjective effects. We studied the interaction of ethanol and acetaminophen, a PGSI, in a double-blind crossover experiment. Six adult males were given no drug or acetaminophen (0, 325, 650, 1300 or 1950 mg) 75 min before ethanol (total dose = 0.625 g/kg; five divided doses). Physiologic, subjective and performance measures were collected. Compared to the no drug condition, ethanol significantly increased ratings of drug "liking," "drunk," "sluggish" and "drug strength" and decreased ratings of "sober." Ethanol increased heart rate and acetaminophen did not diminish or enhance this effect. The failure to antagonize ethanol-induced subjective and physiologic effects by acetaminophen in humans may be due to species differences or inadequate dosage of the PGSI. It is also possible that subjective and certain physiologic effects of ethanol in humans are not mediated by prostaglandin-dependent neural processes. Nevertheless, the finding that at greater than typical analgesic doses, acetaminophen failed to prevent subjective effects of ethanol is of clinical significance. PMID:1539069

  2. Ethanol induces calcium influx via the Cch1-Mid1 transporter in Saccharomyces cerevisiae.

    Courchesne, William E; Vlasek, Christopher; Klukovich, Rachel; Coffee, Sara

    2011-05-01

    Yeast suffers from a variety of environmental stresses, such as osmotic pressure and ethanol produced during fermentation. Since calcium ions are protective for high concentrations of ethanol, we investigated whether Ca(2+) flux occurs in response to ethanol stress. We find that exposure of yeast to ethanol induces a rise in the cytoplasmic concentration of Ca(2+). The response is enhanced in cells shifted to high-osmotic media containing proline, galactose, sorbitol, or mannitol. Suspension of cells in proline and galactose-containing media increases the Ca(2+) levels in the cytoplasm independent of ethanol exposure. The enhanced ability for ethanol to induce Ca(2+) flux after the hypertonic shift is transient, decreasing rapidly over a period of seconds to minutes. There is partial recovery of the response after zymolyase treatment, suggesting that cell wall integrity affects the ethanol-induced Ca(2+) flux. Acetate inhibits the Ca(2+) accumulation elicited by the ethanol/osmotic stress. The Ca(2+) flux is primarily via the Cch1 Ca(2+) influx channel because strains carrying deletions of the cch1 and mid1 genes show greater than 90% reduction in Ca(2+) flux. Furthermore, a functional Cch1 channel reduced growth inhibition by ethanol. PMID:21259000

  3. Role of gamma-irradiated Rosemary against Ethanol Induced Liver Injury in Rats

    Among natural antioxidants, rosemary contains several antioxidant oil and phenolic compounds that may be possessed hepato protective effect. This study aimed to investigate the effect of dietary supplementation with gamma irradiated rosemary on ethanol induced liver injury in rats. Rosemary essential oil was analyzed by gas chromatography/mass spectrometry (GC/MS). The results of biological study revealed that dietary supplementation of either raw or gamma-irradiated rosemary following ethanol administration exerts remarkable modulating effect by reducing the level of total bilirubin, the activity of transaminases, gamma glutamyl transferase and serum alkaline phosphatase, decreasing the concentration of some lipid fractions and malondialdehyde content and xanthine oxidase activity. Also, supplementation of dietary rosemary induced an increase of high density lipoprotein and reduced glutathione content and enhances the activity of xanthine dehydrogenase, superoxide dismutase and catalase activities. Thus, gamma-irradiated rosemary could be incorporated to the diet as a nutritional supplement, to augment the liver's defenses against oxidative stress

  4. Participation of the cholinergic system in the ethanol-induced suppression of paradoxical sleep in rats

    L.A. Papale

    2008-09-01

    Full Text Available Sleep disturbance is among the many consequences of ethanol abuse in both humans and rodents. Ethanol consumption can reduce REM or paradoxical sleep (PS in humans and rats, respectively. The first aim of this study was to develop an animal model of ethanol-induced PS suppression. This model administered intragastrically (by gavage to male Wistar rats (3 months old, 200-250 g 0.5 to 3.5 g/kg ethanol. The 3.5 g/kg dose of ethanol suppressed the PS stage compared with the vehicle group (distilled water during the first 2-h interval (0-2 h; 1.3 vs 10.2; P < 0.001. The second aim of this study was to investigate the mechanisms by which ethanol suppresses PS. We examined the effects of cholinergic drug pretreatment. The cholinergic system was chosen because of the involvement of cholinergic neurotransmitters in regulating the sleep-wake cycle. A second set of animals was pretreated with 2.5, 5.0, and 10 mg/kg pilocarpine (cholinergic agonist or atropine (cholinergic antagonist. These drugs were administered 1 h prior to ethanol (3.5 g/kg or vehicle. Treatment with atropine prior to vehicle or ethanol produced a statistically significant decrease in PS, whereas pilocarpine had no effect on minutes of PS. Although the mechanism by which ethanol induces PS suppression is not fully understood, these data suggest that the cholinergic system is not the only system involved in this interaction.

  5. Ameliorative effect of Opuntia ficus indica juice on ethanol-induced oxidative stress in rat erythrocytes.

    Alimi, Hichem; Hfaeidh, Najla; Bouoni, Zouhour; Sakly, Mohsen; Rhouma, Khémais Ben

    2013-05-01

    The aim of the present study was to investigate the efficacy of Opuntia ficus indica f. inermis fruit juice (OFIj) on reversing oxidative damages induced by chronic ethanol intake in rat erythrocytes. OFIj was firstly analyzed with HPLC for phenolic and flavonoids content. Secondly, 40 adult male Wistar rats were equally divided into five groups and treated for 90 days as follows: control (C), ethanol-only 3 g/kg body weight (b.w) (E), low dose of OFIj 2 ml/100 g b.w+ethanol (Ldj+E), high dose of OFIj 4 ml/100 g b.w+ethanol (Hdj+E), and only a high dose of OFIj 4 ml/100g b.w (Hdj). HPLC analysis indicated high concentrations of phenolic acids and flavonoids in OFIj. Ethanol treatment markedly decreased the activities of erythrocyte superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), and the level of reduced glutathione (GSH). Changes in the erythrocyte's antioxidant ability were accompanied by enhanced oxidative modification of lipids (increase of malondialdeyde level) and proteins (increase in carbonyl groups). Interestingly, pre-administration of either 2 ml/100 g b.w or 4 ml/100 g b.w of OFIj to ethanol-intoxicated rats significantly reversed decreases in enzymatic as well as non enzymatic antioxidants parameters in erythrocytes. Also, the administration of OFIj significantly protected lipids and proteins against ethanol-induced oxidative modifications in rat erythrocytes. The beneficial effect of OFIj can result from the inhibition of ethanol-induced free radicals chain reactions in rat erythrocytes or from the enhancement of the endogenous antioxidants activities. PMID:22285760

  6. Blockade of store-operated calcium entry alleviates ethanol-induced hepatotoxicity via inhibiting apoptosis

    Extracellular Ca2+ influx has been suggested to play a role in ethanol-induced hepatocyte apoptosis and necrosis. Previous studies indicated that store-operated Ca2+ entry (SOCE) was involved in liver injury induced by ethanol in HepG2 cells. However, the mechanisms underlying liver injury caused by SOCE remain unclear. We aimed to investigate the effects and mechanism of SOCE inhibition on liver injury induced by ethanol in BRL cells and Sprague–Dawley rats. Our data demonstrated that ethanol (0–400 mM) dose-dependently increased hepatocyte injury and 100 mM ethanol significantly upregulated the mRNA and protein expression of SOC for at least 72 h in BRL cells. Blockade of SOCE by pharmacological inhibitors and sh-RNA knockdown of STIM1 and Orai1 attenuated intracellular Ca2+ overload, restored the mitochondrial membrane potential (MMP), decreased cytochrome C release and inhibited ethanol-induced apoptosis. STIM1 and Orai1 expression was greater in ethanol-treated than control rats, and the SOCE inhibitor corosolic acid ameliorated the histopathological findings and alanine transaminase and aspartate transaminase activity as well as decreased cytochrome C release and inhibited alcohol-induced cell apoptosis. These findings suggest that SOCE blockade could alleviate alcohol-induced hepatotoxicity via inhibiting apoptosis. SOCE might be a useful therapeutic target in alcoholic liver diseases. - Highlights: • Blockade of SOCE alleviated overload of Ca2+ and hepatotoxicity after ethanol application. • Blockade of SOCE inhibited mitochondrial apoptosis after ethanol application. • SOCE might be a useful therapeutic target in alcoholic liver diseases

  7. Protective potential ofα-tocopherol supplementation against ethanol-induced dysmorphogenesis in postimplantation murine embryos

    SiaAleli JillianL; RamosGliceriaB; deVeraMiriamP

    2015-01-01

    Objective:To assess the protective potential ofα-tocopherol on ethanol-induced dysmorphogenesis in 10.5 embryonic day (ED) mouse embryos.Methods: Forty female mice were randomly assigned into control (CON), positive control (ETOH), low-, medium and high-α-tocopherol-supplemented-Ethanol groups (LTOC, MTOC, HTOC respectively). CON received drinking water without ethanol, ETOH LTOC, MTOC and HTOC groups received 20% ethanol in drinking water. The supplemented groups were given respective dosages ofα-tocopherol, 0.410, 0.819 and 1.640 mg/g body weight, at 14 days before mating until the 9th day of gestation. The 10.5 ED embryos were assessed for embryo weight, head- and crown-rump length, and morphological scoring of brain and sensory vesicles, flexion and somites. The embryo yield was assessed by counting the number of full-term developed embryos from the bulging implantation sites while resorption was assessed by counting the bulging implantation sites but without formed embryos.Results:The weight and head- and crown-rump length of the embryos from theα-tocopherol supplemented groups were comparable to the control. These were significantly higher than that of positive control (P<0.05). Overall morphological scores of the hindbrain and sensory vesicles were significantly higher in the supplemented and control groups than that of the positive control (P<0.05). The number of full-term developed embryos was neither affected by ethanol alone nor with supplementation withα-tocopherol. Resorption was significantly lower in the supplemented groups than that of positive control (P<0.05).Conclusion:The medium and high dosages ofα-tocopherol exhibited a protective effect on ethanol-induced dysmorphogenesis.

  8. Blockade of store-operated calcium entry alleviates ethanol-induced hepatotoxicity via inhibiting apoptosis

    Cui, Ruibing [Department of Hepatology and Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong Province 250012 (China); Yan, Lihui [Shandong Normal University, Jinan, Shandong Province 250012 (China); Luo, Zheng; Guo, Xiaolan [Department of Hepatology and Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong Province 250012 (China); Yan, Ming, E-mail: ymylh@163.com [Department of Hepatology and Gastroenterology, Qilu Hospital of Shandong University, Jinan, Shandong Province 250012 (China)

    2015-08-15

    Extracellular Ca{sup 2+} influx has been suggested to play a role in ethanol-induced hepatocyte apoptosis and necrosis. Previous studies indicated that store-operated Ca{sup 2+} entry (SOCE) was involved in liver injury induced by ethanol in HepG2 cells. However, the mechanisms underlying liver injury caused by SOCE remain unclear. We aimed to investigate the effects and mechanism of SOCE inhibition on liver injury induced by ethanol in BRL cells and Sprague–Dawley rats. Our data demonstrated that ethanol (0–400 mM) dose-dependently increased hepatocyte injury and 100 mM ethanol significantly upregulated the mRNA and protein expression of SOC for at least 72 h in BRL cells. Blockade of SOCE by pharmacological inhibitors and sh-RNA knockdown of STIM1 and Orai1 attenuated intracellular Ca{sup 2+} overload, restored the mitochondrial membrane potential (MMP), decreased cytochrome C release and inhibited ethanol-induced apoptosis. STIM1 and Orai1 expression was greater in ethanol-treated than control rats, and the SOCE inhibitor corosolic acid ameliorated the histopathological findings and alanine transaminase and aspartate transaminase activity as well as decreased cytochrome C release and inhibited alcohol-induced cell apoptosis. These findings suggest that SOCE blockade could alleviate alcohol-induced hepatotoxicity via inhibiting apoptosis. SOCE might be a useful therapeutic target in alcoholic liver diseases. - Highlights: • Blockade of SOCE alleviated overload of Ca{sup 2+} and hepatotoxicity after ethanol application. • Blockade of SOCE inhibited mitochondrial apoptosis after ethanol application. • SOCE might be a useful therapeutic target in alcoholic liver diseases.

  9. Antioxidant Mechanism is Involved in the Gastroprotective Effects of Ozonized Sunflower Oil in Ethanol-Induced Ulcers in Rats

    Zullyt B. Zamora Rodríguez

    2007-01-01

    In summary, our results demonstrate that OSO pretreatment exerts protective effects in ethanol-induced gastric ulcers in rats. Furthermore, these results provide evidence that these protective effects of OSO are mediated at least partially by stimulation of some important antioxidant enzymes such as SOD and GSH-Px, which are scavengers of ROS and therefore prevent gastric injury induced by them.

  10. Cyanidin-3-Glucoside inhibits ethanol-induced invasion of breast cancer cells overexpressing ErbB2

    Wang Shiow

    2010-10-01

    Full Text Available Abstract Background Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-glucoside (C3G, an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS. This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion. Results C3G attenuated ethanol-induced migration/invasion of breast cancer cells expressing high levels of ErbB2 (BT474, MDA-MB231 and MCF7ErbB2 in a concentration dependent manner. C3G decreased ethanol-mediated cell adhesion to the extracellular matrix (ECM as well as the amount of focal adhesions and the formation of lamellipodial protrusion. It inhibited ethanol-stimulated phosphorylation of ErbB2, cSrc, FAK and p130Cas, as well as interactions among these proteins. C3G abolished ethanol-mediated p130Cas/JNK interaction. Conclusions C3G blocks ethanol-induced activation of the ErbB2/cSrc/FAK pathway which is necessary for cell migration/invasion. C3G may be beneficial in preventing/reducing ethanol-induced breast cancer metastasis.

  11. Apocynin protects against ethanol-induced gastric ulcer in rats by attenuating the upregulation of NADPH oxidases 1 and 4.

    El-Naga, Reem N

    2015-12-01

    Gastric ulcer is a common gastrointestinal disorder affecting many people all over the world. Absolute ethanol (5 ml/kg) was used to induce gastric ulceration in rats. Apocynin (50 mg/kg) was given orally one hour before the administration of absolute ethanol. Omeprazole (20 mg/kg) was used as a standard. Interestingly, apocynin pre-treatment provided 93.5% gastroprotection against ethanol-induced ulceration. Biochemically, gastric mucin content was significantly increased with apocynin pre-treatment. This finding was further supported by alcian blue staining of stomach sections obtained from the different treated groups. Also, gastric juice volume and acidity were significantly reduced. Apocynin significantly ameliorated ethanol-induced oxidative stress by replenishing reduced glutathione and superoxide dismutase levels as well as reducing elevated malondialdehyde levels in gastric tissues. Besides, ethanol-induced pro-inflammatory response was significantly decreased by apocynin pre-treatment via reducing elevated levels of pro-inflammatory markers; interleukin-1β, tumor necrosis factor-α, cyclooxygenase-2 and inducible nitric oxide synthase. Additionally, caspase-3 tissue level was significantly reduced in apocynin pre-treated group. Interestingly, NADPH oxidase-1 (NOX-1) and NOX-4 up-regulation was shown to be partially involved in the pathogenesis of ethanol-induced gastric ulceration and was significantly reversed by apocynin pre-treatment. Gastroprotective properties of apocynin were confirmed by histopathological examination. It is worth mentioning that apocynin was superior in all aspects except gastric mucin content parameter where it was significantly increased by 13.5 folds in the omeprazole pre-treated group. This study was the first to show that apocynin is a promising gastroprotective agent against ethanol-induced gastric ulceration, partially via its anti-oxidant, anti-inflammatory, anti-apoptotic effects as well as down-regulating NOX-1 and NOX-4

  12. Neuroprotection with metformin and thymoquinone against ethanol-induced apoptotic neurodegeneration in prenatal rat cortical neurons

    Ullah Ikram

    2012-01-01

    Full Text Available Abstract Background Exposure to ethanol during early development triggers severe neuronal death by activating multiple stress pathways and causes neurological disorders, such as fetal alcohol effects or fetal alcohol syndrome. This study investigated the effect of ethanol on intracellular events that predispose developing neurons for apoptosis via calcium-mediated signaling. Although the underlying molecular mechanisms of ethanol neurotoxicity are not completely determined, mitochondrial dysfunction, altered calcium homeostasis and apoptosis-related proteins have been implicated in ethanol neurotoxicity. The present study was designed to evaluate the neuroprotective mechanisms of metformin (Met and thymoquinone (TQ during ethanol toxicity in rat prenatal cortical neurons at gestational day (GD 17.5. Results We found that Met and TQ, separately and synergistically, increased cell viability after ethanol (100 mM exposure for 12 hours and attenuated the elevation of cytosolic free calcium [Ca2+]c. Furthermore, Met and TQ maintained normal physiological mitochondrial transmembrane potential (ΔψM, which is typically lowered by ethanol exposure. Increased cytosolic free [Ca2+]c and lowered mitochondrial transmembrane potential after ethanol exposure significantly decreased the expression of a key anti-apoptotic protein (Bcl-2, increased expression of Bax, and stimulated the release of cytochrome-c from mitochondria. Met and TQ treatment inhibited the apoptotic cascade by increasing Bcl-2 expression. These compounds also repressed the activation of caspase-9 and caspase-3 and reduced the cleavage of PARP-1. Morphological conformation of cell death was assessed by TUNEL, Fluoro-Jade-B, and PI staining. These staining methods demonstrated more cell death after ethanol treatment, while Met, TQ or Met plus TQ prevented ethanol-induced apoptotic cell death. Conclusion These findings suggested that Met and TQ are strong protective agents against ethanol-induced

  13. Role of Nrf2 in preventing ethanol-induced oxidative stress and lipid accumulation

    Oxidative stress and lipid accumulation play important roles in alcohol-induced liver injury. Previous reports showed that, in livers of nuclear factor erythroid 2-related factor 2 (Nrf2)-activated mice, genes involved in antioxidant defense are induced, whereas genes involved in lipid biosynthesis are suppressed. To investigate the role of Nrf2 in ethanol-induced hepatic alterations, Nrf2-null mice, wild-type mice, kelch-like ECH-associated protein 1-knockdown (Keap1-KD) mice with enhanced Nrf2, and Keap1-hepatocyte knockout (Keap1-HKO) mice with maximum Nrf2 activation, were treated with ethanol (5 g/kg, po). Blood and liver samples were collected 6 h thereafter. Ethanol increased alanine aminotransferase and lactate dehydrogenase activities as well as thiobarbituric acid reactive substances in serum of Nrf2-null and wild-type mice, but not in Nrf2-enhanced mice. After ethanol administration, mitochondrial glutathione concentrations decreased markedly in Nrf2-null mice but not in Nrf2-enhanced mice. H2DCFDA staining of primary hepatocytes isolated from the four genotypes of mice indicates that oxidative stress was higher in Nrf2-null cells, and lower in Nrf2-enhanced cells than in wild-type cells. Ethanol increased serum triglycerides and hepatic free fatty acids in Nrf2-null mice, and these increases were blunted in Nrf2-enhanced mice. In addition, the basal mRNA and nuclear protein levels of sterol regulatory element-binding protein 1(Srebp-1) were decreased with graded Nrf2 activation. Ethanol further induced Srebp-1 mRNA in Nrf2-null mice but not in Nrf2-enhanced mice. In conclusion, Nrf2 activation prevented alcohol-induced oxidative stress and accumulation of free fatty acids in liver by increasing genes involved in antioxidant defense and decreasing genes involved in lipogenesis. -- Highlights: ► Ethanol depleted mitochondrial GSH in Nrf2-null mice but not in Keap1-KD mice. ► Ethanol increased ROS in hepatocytes isolated from Nrf2-null and wild

  14. Induction of Heme Oxygenase-1 in Human Hepatocytes to Protect Them From Ethanol-induced Cytotoxicity

    LIE-GANG LIU; HONG YAN; WEN ZHANG; PING YAO; XI-PING ZHANG; XIU-FA SUN; ANDREAS K. NUSSLER

    2004-01-01

    We investigated the relationship between ethanol exposure and heme oxygenase (HO-1) in human hepatocytes in order to ascertain if induction of HO-1 can prevent ethanol induced cellular damage. Methods Dose-dependent (25-100 mmol/L) and time-dependent (0-24 h) ethanol exposure were used in the present study. HO-1 mRNA and protein expression were detected by PT-PCR and Western blot respectively. HO-1 activity was indicated by bilirubin and Fe2+ formation. Cytotoxicity was investigated by means of lactate dehydrogenate (LDH) and aspartate transaminase (AST) level in culture supernatants, as well as the intracellular formation of malondialdehyde (MDA), cellular glutathione (GSH) status and CYP 2E1 activity. Results We first demonstrated a dose-dependent response between ethanol exposure and HO-1 mRNA and protein expression in human hepatocytes. We further observed a time-dependent increase of HO-1 mRNA expression using 100 mmol/L ethanol starting 30 minutes after ethanol exposure, reaching its maximum between 3 h and 9 h. Being similar to what had been demonstrated with the mRNA level, increased protein expression started at 6 h after ethanol exposure, and kept continuous elevated over 18 h. In addition, we found that ethanol exposure to hepatocytes markedly increased HO-1 enzyme activity in a time-dependent manner measured as bilirubin and Fe2+ formation in human hepatocytes. Our results clearly showed that ethanol exposure caused a significant increase of LDH, AST, and MDA levels, while the antioxidant GSH was time-dependently reduced. Furthermore, we demonstrated that pre-administration of cobalt protoporphyrin (CoPP) induced HO-1 in human hepatocytes, and prevented an increase of MDA and a decrease of GSH. These effects could be partially reversed by zinc protoporphyrin (ZnPP), an antagonist of HO-1 induction. Conclusion HO-1 expression in cells or organs could lead to new strategies for better prevention and treatment of ethanol-induced oxidative damage in human

  15. Inhibition of phosphorylated tyrosine hydroxylase attenuates ethanol-induced hyperactivity in adult zebrafish (Danio rerio).

    Nowicki, Magda; Tran, Steven; Chatterjee, Diptendu; Gerlai, Robert

    2015-11-01

    Zebrafish have been successfully employed in the study of the behavioural and biological effects of ethanol. Like in mammals, low to moderate doses of ethanol induce motor hyperactivity in zebrafish, an effect that has been attributed to the activation of the dopaminergic system. Acute ethanol exposure increases dopamine (DA) in the zebrafish brain, and it has been suggested that tyrosine hydroxylase, the rate-limiting enzyme of DA synthesis, may be activated in response to ethanol via phosphorylation. The current study employed tetrahydropapaveroline (THP), a selective inhibitor of phosphorylated tyrosine hydroxylase, for the first time, in zebrafish. We treated zebrafish with a THP dose that did not alter baseline motor responses to examine whether it can attenuate or abolish the effects of acute exposure to alcohol (ethanol) on motor activity, on levels of DA, and on levels of dopamine's metabolite 3,4-dihydroxyphenylacetic acid (DOPAC). We found that 60-minute exposure to 1% alcohol induced motor hyperactivity and an increase in brain DA. Both of these effects were attenuated by pre-treatment with THP. However, no differences in DOPAC levels were found among the treatment groups. These findings suggest that tyrosine hydroxylase is activated via phosphorylation to increase DA synthesis during alcohol exposure in zebrafish, and this partially mediates alcohol's locomotor stimulant effects. Future studies will investigate other potential candidates in the molecular pathway to further decipher the neurobiological mechanism that underlies the stimulatory properties of this popular psychoactive drug. PMID:26366782

  16. Ethanol induced astaxanthin accumulation and transcriptional expression of carotenogenic genes in Haematococcus pluvialis.

    Wen, Zewen; Liu, Zhiyong; Hou, Yuyong; Liu, Chenfeng; Gao, Feng; Zheng, Yubin; Chen, Fangjian

    2015-10-01

    Haematococcus pluvialis is one of the most promising natural sources of astaxanthin. However, inducing the accumulation process has become one of the primary obstacles in astaxanthin production. In this study, the effect of ethanol on astaxanthin accumulation was investigated. The results demonstrated that astaxanthin accumulation occurred with ethanol addition even under low-light conditions. The astaxanthin productivity could reach 11.26 mg L(-1) d(-1) at 3% (v/v) ethanol, which was 2.03 times of that of the control. The transcriptional expression patterns of eight carotenogenic genes were evaluated using real-time PCR. The results showed that ethanol greatly enhanced transcription of the isopentenyl diphosphate (IPP) isomerase genes (ipi-1 and ipi-2), which were responsible for isomerization reaction of IPP and dimethylallyl diphosphate (DMAPP). This finding suggests that ethanol induced astaxanthin biosynthesis was up-regulated mainly by ipi-1 and ipi-2 at transcriptional level, promoting isoprenoid synthesis and substrate supply to carotenoid formation. Thus ethanol has the potential to be used as an effective reagent to induce astaxanthin accumulation in H. pluvialis. PMID:26215339

  17. The relationship between ethanol-induced hyperglycemia and hypothermia: evidence of genetic correlation.

    Risinger, F O; Cunningham, C L

    1991-08-01

    The hyperglycemic and hypothermic responses to acute ethanol exposure (0, 2, 4, 6 g/kg, intraperitoneally) were examined in non-fasted mice selectively bred for sensitivity (COLD line) or insensitivity (HOT line) to ethanol-induced hypothermia. Blood samples and rectal temperatures were obtained immediately before injection and hourly for 4 hr after injection. As expected, COLD mice demonstrated greater and more prolonged reductions in body temperature than HOT mice, especially at the 4 g/kg dose (HOT: -2.58 degrees C, COLD: -5.08 degrees C). Ethanol produced significant dose-dependent elevations in blood glucose levels over the 4-hr sampling period in both lines. The greatest elevations in blood glucose levels were seen at 4 g/kg, with COLD mice (mean = 225.1 mg/dl) showing significantly greater elevations in blood glucose levels compared to HOT mice (mean = 177.0 mg/dl). These results support the hypothesis that the thermic and glycemic effects produced by ethanol are due to related neural processes that share a common genetic component. PMID:1928651

  18. The Protective Role of Zinc Sulphate on Ethanol -Induced Liver and Kidney Damages in Rats

    Around the world more and more people suffer from alcoholism. Addiction problems, alcoholism and excessive use of drugs both medical and nonmedical, are major causes of liver and kidney damage in adults. The purpose of this study was to investigate on the protective role of zinc sulphate on liver and kidney in rats with acute alcoholism. Wistar albino rats were divided into four groups. Group I; control group, group 2; given only Zinc Sulphate (100 mg/kg/day for 3days), group 3; rats given absolute ethanol (1 ml of absolute ethanol administrated by gavage technique to each rat), group 4 given Zinc sulphate prior to the administration of absolute ethanol. The results of this study revealed that acute ethanol exposure caused degenerative morphological changes in the liver and kidney. Significant difference were found in the levels of serum, liver, kidney super oxide dismutase(SOD), catalase (CAT), nitric oxide(NO), and malondialdehyde (MDA) in the ethanol group compared to the control group. Moreover ,serum urea, creatnine, uric acid, alkaline phoshpatase and transaminases activities (GOTand GPT) were increased in the ethanol group compared to the control group. On the other hand,administration of zinc sulphate in the ethanol group caused a significant decrease in the degenerative changes, lipid peroxidation, antioxidant enzymes, and nitric oxide in serum, liver, and kidney. It can be concluded that zinc Sulphate has a protective role on the ethanol induced liver and kidney injury. In addition ,nitric oxide is involved in the mechanism of acute alcohol intoxication. (author)

  19. The Zebrafish, a Novel Model Organism for Screening Compounds Affecting Acute and Chronic Ethanol-Induced Effects.

    Tran, S; Facciol, A; Gerlai, R

    2016-01-01

    Alcohol addiction is a major unmet medical and economic issue for which very few efficacious pharmacological treatment options are currently available. The development and identification of new compounds and drugs to treat alcohol addiction is hampered by the high costs and low amenability of traditional laboratory rodents to high-throughput behavioral screens. The zebrafish represents an excellent compromise between systems complexity and practical simplicity by overcoming many limitations inherent in these rodent models. In this chapter, we review current advances in the behavioral and neurochemical characterization of ethanol-induced changes in zebrafish. We also discuss the basic principles and methods of and the most recent advances in using paradigms with which one can screen for compounds altering acute and chronic ethanol-induced effects in zebrafish. PMID:27055623

  20. Differential effects of ethanol antagonism and neuroprotection in peptide fragment NAPVSIPQ prevention of ethanol-induced developmental toxicity

    Wilkemeyer, Michael F.; Chen, Shao-Yu; Menkari, Carrie E.; Brenneman, Douglas E.; Sulik, Kathleen K.; Charness, Michael E.

    2003-01-01

    NAPVSIPQ (NAP), an active fragment of the glial-derived activity-dependent neuroprotective protein, is protective at femtomolar concentrations against a wide array of neural insults and prevents ethanol-induced fetal wastage and growth retardation in mice. NAP also antagonizes ethanol inhibition of L1-mediated cell adhesion (ethanol antagonism). We performed an Ala scanning substitution of NAP to determine the role of ethanol antagonism and neuroprotection in NAP preve...

  1. Acute Toxicity and Gastroprotective Role of M. pruriens in Ethanol-Induced Gastric Mucosal Injuries in Rats

    Shahram Golbabapour; Maryam Hajrezaie; Pouya Hassandarvish; Nazia Abdul Majid; A. Hamid A. Hadi; Noraziah Nordin; Mahmood A. Abdulla

    2013-01-01

    The investigation was to evaluate gastroprotective effects of ethanolic extract of M. pruriens leaves on ethanol-induced gastric mucosal injuries in rats. Forty-eight rats were divided into 8 groups: negative control, extract control, ulcer control, reference control, and four experimental groups. As a pretreatment, the negative control and the ulcer control groups were orally administered carboxymethylcellulose (CMC). The reference control was administered omeprazole orally (20 mg/kg). The e...

  2. Effects of Pithecellobium Jiringa Ethanol Extract against Ethanol-Induced Gastric Mucosal Injuries in Sprague-Dawley Rats

    Fouad Hussain AL-Bayaty; Siddig Ibrahim Abdelwahab; Nimir, Amal R.; Suhailah Wasmn Qader; Mahmood Ameen Abdulla; Ibrahim Abdel Aziz Ibrahim

    2012-01-01

    Current anti-gastric ulcer agents have side effects, despite the progression and expansion of advances in treatment. This study aimed to investigate the gastroprotective mechanisms of Pithecellobium jiringa ethanol extract against ethanol-induced gastric mucosal ulcers in rats. For this purpose, Sprague Dawley rats were randomly divided into five groups: Group 1 (normal control) rats were orally administered with vehicle (carboxymethyl cellulose), Group 2 (ulcer control) rats were also orally...

  3. Myocardial Bridging

    Shi-Min Yuan

    2016-02-01

    Full Text Available Abstract Myocardial bridging is rare. Myocardial bridges are most commonly localized in the middle segment of the left anterior descending coronary artery. The anatomic features of the bridges vary significantly. Alterations of the endothelial morphology and the vasoactive agents impact on the progression of atherosclerosis of myocardial bridging. Patients may present with chest pain, myocardial infarction, arrhythmia and even sudden death. Patients who respond poorly to the medical treatment with β-blockers warrant a surgical intervention. Myotomy is a preferred surgical procedure for the symptomatic patients. Coronary stent deployment has been in limited use due to the unsatisfactory long-term results.

  4. Myocardial Bridge

    ... Myocarditis Obstructive Sleep Apnea Pericarditis Peripheral Vascular Disease Rheumatic ... Related terms: myocardium, coronary arteries, myocardial ischemia Your heart is made of muscle, called the myocardium. The ...

  5. Myocardial Bridging.

    Yuan, Shi-Min

    2016-02-01

    Myocardial bridging is rare. Myocardial bridges are most commonly localized in the middle segment of the left anterior descending coronary artery. The anatomic features of the bridges vary significantly. Alterations of the endothelial morphology and the vasoactive agents impact on the progression of atherosclerosis of myocardial bridging. Patients may present with chest pain, myocardial infarction, arrhythmia and even sudden death. Patients who respond poorly to the medical treatment with β-blockers warrant a surgical intervention. Myotomy is a preferred surgical procedure for the symptomatic patients. Coronary stent deployment has been in limited use due to the unsatisfactory long-term results. PMID:27074276

  6. Hepatoprotective effect of Piper guineense aqueous extract against ethanol-induced toxicity in male rats

    Babatunji E. Oyinloye

    2012-02-01

    Full Text Available Objective: Herbal medicinal products play an important role in the management of liver diseases for the lack of satisfactory liver protective drugs in allopathic medical practices. Searching for hepatoprotective drugs with high efficacy and safety is of great need. Our aim is to evaluate the hepatoprotective and antioxidant effect of aqueous extract of Piper guineense (P.G. on ethanol induced toxicity in Wistar rats. Methods: In order to assess the hepatoprotective effect of this extract in experimental animals, twenty-four Wistar male albino rats (weighing 150-170 g were divided into four groups. Toxicity was induced by administering 45% ethanol (4.8 g/kg b.w by oral gavage for 21 days. Serum triglyceride (TG levels, alanine aminotransferase (ALT and aspartate aminotransferase (AST activities were monitored. Thiobarbituric acid reactive substances, reduced glutathione (GSH levels, superoxide dismutase (SOD and gluthathione-S-transferase (GST activities were determined in the liver. Results: At the end of the experiment, chronic administration of ethanol resulted in enhanced lipid peroxidation (LPO with depletion in the levels of GSH as well as reduction in the activities of SOD and GST. TG levels, ALT and AST activities were elevated. This was attenuated by the co-administration of the P.guineense extract by oral gavage (100 or 200 mg/kg b.w. Administration of the plant extract during ethanol exposure inhibited hepatic LPO and ameliorated SOD and GST activities as well as restoring GSH levels significantly. Conclusion: From this study it can be concluded that aqueous extract of P.guineense possess some potent antioxidants which can ameliorate hepatic damage associated with chronic ethanol exposure in rat models. [J Exp Integr Med 2012; 2(1.000: 71-76

  7. Effect of the fractions of Coccinia grandis on Ethanol-Induced cerebral oxidative stress in rats

    M Umamaheswari

    2009-01-01

    Full Text Available The present study was aimed at investigating the effect of the various fractions of hydromethanol extract of the leaves of Coccinia grandis (Cucurbitaceae against ethanol-induced cerebral oxidative stress in rats. The leaves of this species is used in traditional medicine for treating jaundice, bronchitis, skin eruptions, burns, rheumatism, syphilis, gonorrhoea, etc. Cerebral oxidative stress was induced in rats by the administration of 20% ethanol (5 ml/100 g b.w. for 28 days. The pet-ether (PEF, chloroform (CF, ethylacetate (EAF and residual (RF fractions at a dose of 200 mg/kg b.w. were simultaneously administered with ethanol orally for 28 days. Vitamin E at a dose of 100 mg/kg orally was used as the standard. Administration of ethanol resulted in a significant increase in the activities of serum transaminases, alkaline phosphatase, uric acid and lipid levels. In addition, there was a significant elevation in the levels of malondialdehyde and lipid hydroperoxides and a reduction in the activities of enzymatic and non-enzymatic antioxidants in the brain. Simultaneous administration of the fractions prevented the enzymatic leakage and the rise in uric acid and lipid levels. All the fractions (except the residual fraction prevented the peroxidative damage caused by ethanol, which is evidenced from the improved antioxidant potential. Further, histopathological examination of the brain tissue revealed that the fractions offered significant protection against ethanol toxicity. Among the fractions tested, the chloroform fraction exhibited appreciable antioxidant property, which was almost comparable with the standard Vitamin E. These results suggest that the leaves of Coccinia grandis exhibit significant antioxidant activity in ethanol-treated rats.

  8. Molecular mechanisms of ethanol-induced pathogenesis revealed by RNA-sequencing.

    Laura Camarena

    2010-04-01

    Full Text Available Acinetobacter baumannii is a common pathogen whose recent resistance to drugs has emerged as a major health problem. Ethanol has been found to increase the virulence of A. baumannii in Dictyostelium discoideum and Caenorhabditis elegans models of infection. To better understand the causes of this effect, we examined the transcriptional profile of A. baumannii grown in the presence or absence of ethanol using RNA-Seq. Using the Illumina/Solexa platform, a total of 43,453,960 reads (35 nt were obtained, of which 3,596,474 mapped uniquely to the genome. Our analysis revealed that ethanol induces the expression of 49 genes that belong to different functional categories. A strong induction was observed for genes encoding metabolic enzymes, indicating that ethanol is efficiently assimilated. In addition, we detected the induction of genes encoding stress proteins, including upsA, hsp90, groEL and lon as well as permeases, efflux pumps and a secreted phospholipase C. In stationary phase, ethanol strongly induced several genes involved with iron assimilation and a high-affinity phosphate transport system, indicating that A. baumannii makes a better use of the iron and phosphate resources in the medium when ethanol is used as a carbon source. To evaluate the role of phospholipase C (Plc1 in virulence, we generated and analyzed a deletion mutant for plc1. This strain exhibits a modest, but reproducible, reduction in the cytotoxic effect caused by A. baumannii on epithelial cells, suggesting that phospholipase C is important for virulence. Overall, our results indicate the power of applying RNA-Seq to identify key modulators of bacterial pathogenesis. We suggest that the effect of ethanol on the virulence of A. baumannii is multifactorial and includes a general stress response and other specific components such as phospholipase C.

  9. Hepatoprotective Evaluation of Ganoderma lucidum Pharmacopuncture: In vivo Studies of Ethanol-induced Acute Liver Injury

    Sun-Hee Jang

    2014-09-01

    Full Text Available Objectives: Alcohol abuse is a public issue and one of the major causes of liver disease worldwide. This study was aimed at investigating the protective effect of Ganoderma lucidum pharmacopuncture (GLP against hepatotoxicity induced by acute ethanol (EtOH intoxication in rats. Methods: Sprague-Dawley (SD rats were divided into 4 groups of 8 animals each: normal, control, normal saline pharmacopuncture (NP and GLP groups. The control, NP and GLP groups received ethanol orally. The NP and the GLP groups were treated daily with injections of normal saline and Ganoderma lucidum extract, respectively. The control group received no treatment. The rats in all groups, except the normal group, were intoxicated for 6 hours by oral administration of EtOH (6 g/kg BW. The same volume of distilled water was administered to the rats in the normal group. Two local acupoints were used: Qimen (LR14 and Taechung (LR3. A histopathological analysis was performed, and the liver function and the activities of antioxidant enzymes were assessed. Results: GLP treatment reduced the histological changes due to acute liver injury induced by EtOH and significantly reduced the increase in the alanine aminotransferase (ALT enzyme; however, it had an insignificant effect in reducing the increase in aspartate aminotransferase (AST enzyme. It also significantly ameliorated the superoxide dismutase (SOD and the catalase (CAT activities. Conclusion: The present study suggests that GLP treatment is effective in protecting against ethanol-induced acute hepatic injury in SD rats by modulating the activities of ethanol metabolizing enzymes and by attenuating oxidative stress.

  10. Ethanol induced mitochondria injury and permeability transition pore opening: Role of mitochondria in alcoholic liver disease

    Ming Yan; Ping Zhu; Hui-Min Liu; Hai-Tao Zhang; Li Liu

    2007-01-01

    AIM: To observe changes of mitochondria and investigate the effect of ethanol on mitochondrial permeability transition pore (PTP), mitochondrial membrane potential (MMP, Δψm) and intracellular calcium concentration in hepatocytes by establishing an animal model of alcoholic liver disease (ALD).METHODS: Fourty adult male Wistar rats were randomly divided into two groups, the model group (20) was administered alcohol intragastrically plus an Oliver oil diet to establish an ALD model, and the control group (20) was given an equal amount of normal saline. The ultramicrostructural changes of mitochondria were observed under electron microscopy. Mitochondria of liver was extracted, and patency of PTP, mitochondrial membrane potential (Δψm), mitochondrial mass and intracellular calcium concentration of isolated hepacytes were detected by flow cytometry using rhodamine123 (Rh123), Nonyl-Acridine Orange and calcium fluorescent probe Fluo-3/AM, respectively.RESULTS: Membrane and cristae were broken or disappeared in mitochondria in different shapes under electron microscopy. Some mitochondria showed U shape or megamitochondrion. In the model group, liver mitochondria PTP was broken, and mitochondria swelled, the absorbance at 450 nm, A540 decreased (0.0136 ± 0.0025 vs 0.0321 ± O.0013,model vs control,P<O.01);mitochondria transmembrane potential (239.4638 ± 12.7263 vs 377.5850 ± 16.8119,P<0.01) was lowered;mitochondrial mass (17.4350 ± 1.9880 vs 31.6738 ± 3.4930,P<0.01);and [Ca2+]i was increased in liver cells (7.0020 ± 0.5008 vs 10.2050 ± 0.4701,P<0.01).CONCLUSION:Chronic alcohol intake might lead to broken mitochondria PTP,decreased mitochondria membrane potential and injury,and elevated intracellular Ca2+ production.Ethanol-induced chondriosome injury may be an important mechanism of alcoholic diseases.

  11. Finland Has it All? Examining the Media Accentuation of "Finnish Education" in Australia, Germany and South Korea

    Takayama, Keita; Waldow, Florian; Sung, Youl-Kwan

    2013-01-01

    Drawing on the conceptual work of externalisation in comparative education and multi-accentual signs in cultural studies, this article examines how the print news media accentuate "Finnish education" in the process of inserting this external reference into the domestic political discourses around education reform in Australia, Germany…

  12. Roles of nitric oxide in protective effect of berberine in ethanol-induced gastric ulcer mice

    Long-rui PAN; Qiang TANG; Qin FU; Ben-rong HU; Ji-zhou XIANG; Jia-qing QIAN

    2005-01-01

    Aim: To investigate the protective effects of berberine on ethanol-induced gastric ulcer in mice. Methods: Gastric ulcers were induced by oral ingestion of ethanol. Nitric oxide (NO) content was measured, and mRNA expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS)were analyzed by reverse transcription-polymerase chain reaction (RT-PCR).Results: The ulcer index (UI) at 1 h, 2 h, 3 h and 6 h after oral administration of ethanol was 23.8± 1.4, 23.3±2.2, 22.3± 1.2 and 20.8± 1.1, respectively. The UI in the berberine-treated groups (5 mg/kg and 50 mg/kg) was less than the control group.The content of NO in the control group was 73.3±7.3 μL/L, 94.0±9.2 μL/L, 109.6±6.4 μL/L and 138.2±10.2 μL/L in gastric juice and 5.8± 1.1 μmol/g protein, 8.3±1.1 μmol/g protein, 9.8± 1.1 μmol/g protein and 11.9± 1.2 μmol/g protein in gastric tissue at 1 h, 2 h, 3 h and 6 h, respectively, after the oral administration of ethanol.The content of NO in the berberine-treated groups (5 mg/kg and 50 mg/kg) was higher than the control group at 1 h after the oral administration of ethanol(P<0.05), and was lower at 6 h (P<0.05). Analysis by RT-PCR showed that expression of eNOS was inhibited but iNOS expression was enhanced by ethanol.However, the expression of eNOS could be enhanced and iNOS expression could be inhibited by berberine (P<0.01). Conclusion: Berberine could significantly protect gastric mucosa from damage by ethanol. This effect may be related to the increased expression of eNOS mRNA and inhibited expression of iNOS mRNA.

  13. Quetiapine mitigates the ethanol-induced oxidative stress in brain tissue, but not in the liver, of the rat

    Han JH

    2015-06-01

    Full Text Available Jin-hong Han,1,2 Hong-zhao Tian,2 Yang-yang Lian,1 Yi Yu,1 Cheng-biao Lu,2 Xin-min Li,3 Rui-ling Zhang,1 Haiyun Xu4 1The Second Affiliated Hospital of Xinxiang Medical University, 2School of Basic Medicine, Xinxiang Medical University, Xinxiang, Henan, People’s Republic of China; 3Department of Psychiatry, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada; 4The Mental Health Center, Shantou University Medical College, Shantou, Guangdong, People’s Republic of China Abstract: Quetiapine, an atypical antipsychotic, has been employed to treat alcoholic patients with comorbid psychopathology. It was shown to scavenge hydroxyl radicals and to protect cultured cells from noxious effects of oxidative stress, a pathophysiological mechanism involved in the toxicity of alcohol. This study compared the redox status of the liver and the brain regions of prefrontal cortex, hippocampus, and cerebellum of rats treated with or without ethanol and quetiapine. Ethanol administration for 1 week induced oxidative stress in the liver and decreased the activity of glutathione peroxidase and total antioxidant capacity (TAC there. Coadministration of quetiapine did not protect glutathione peroxidase and TAC in the liver against the noxious effect of ethanol, thus was unable to mitigate the ethanol-induced oxidative stress there. The ethanol-induced alteration in the redox status in the prefrontal cortex is mild, whereas the hippocampus and cerebellum are more susceptible to ethanol intoxication. For all the examined brain regions, coadministration of quetiapine exerted effective protection on the antioxidants catalase and total superoxide dismutase and on the TAC, thus completely blocking the ethanol-induced oxidative stress in these brain regions. These protective effects may explain the clinical observations that quetiapine reduced psychiatric symptoms intensity and maintained a good level of tolerability in chronic alcoholism with

  14. Protective Effects of the Traditional Herbal Formula Oryeongsan Water Extract on Ethanol-Induced Acute Gastric Mucosal Injury in Rats

    Jeon, Woo-Young; Lee, Mee-Young; Shin, In-Sik; Lim, Hye-Sun; Shin, Hyeun-Kyoo

    2012-01-01

    This study was performed to evaluate the protective effect and safety of Oryeongsan water extract (OSWE) on ethanol-induced acute gastric mucosal injury and an acute toxicity study in rats. Acute gastric lesions were induced via intragastric oral administration of absolute ethanol at a dose of 5 mL/kg. OSWE (100 and 200 mg/kg) was administered to rats 2 h prior to the oral administration of absolute ethanol. The stomach of animal models was opened and gastric mucosal lesions were examined. Ga...

  15. Chronic psychosocial stress causes delayed extinction and exacerbates reinstatement of ethanol-induced conditioned place preference in mice

    Bahi, Amine; Dreyer, Jean-luc

    2014-01-01

    Objective: Here, we examined the impact of chronic subordinate colony (CSC) exposure on EtOH-CPP extinction, as well as ethanol-induced reinstatement of CPP.Methods: Mice were conditioned with saline or 1.5 g/kg ethanol and were tested in the EtOH-CPP model. In the first experiment, the mice were subjected to 19 days of chronic stress, and EtOH-CPP extinction was assessed during seven daily trials without ethanol injection. In the second experiment and after the EtOH-CPP test, the mice were s...

  16. Protective effects of resveratrol on ethanol-induced apoptosis in embryonic stem cells and disruption of embryonic development in mouse blastocysts

    Previous studies have established that ethanol induces apoptosis, but the precise molecular mechanisms are currently unclear. Here, we show that 0.3-1.0% (w/v) ethanol induces apoptosis in mouse blastocysts and that resveratrol, a grape-derived phytoalexin with known antioxidant and anti-inflammatory properties, prevents ethanol-induced apoptosis and inhibition of cell proliferation. Moreover, ethanol-treated blastocysts show normal levels of implantation on culture dishes in vitro but a reduced ability to reach the later stages of embryonic development. Pretreatment with resveratrol prevented ethanol-induced disruption of embryonic development in vitro and in vivo. In an in vitro cell-based assay, we further found that ethanol increases the production of reactive oxygen species in ESC-B5 embryonic stem cells, leading to an increase in the intracellular concentrations of cytoplasmic free Ca2+ and NO, loss of mitochondrial membrane potential, mitochondrial release of cytochrome c, activation of caspase-9 and -3, and apoptosis. These changes were blocked by pretreatment with resveratrol. Based on these results, we propose a model for the protective effect of resveratrol on ethanol-induced cell injury in blastocysts and ESC-B5 cells

  17. Reversing gastric mucosal alterations during ethanol-induced chronic gastritis in rats by oral administration of Opuntia ficus- indica mucilage

    Ricardo Vázquez-Ramírez; Marisela Olguín-Martínez; Carlos Kubli-Garfias; Rolando Hernández-Mu(n)oz

    2006-01-01

    AIM: To study the effect of mucilage obtained from cladodes of Opuntia ficus-indica (Cactaceae) on the healing of ethanol-induced gastritis in rats.METHODS: Chronic gastric mucosa injury was treated with mucilage (5 mg/kg per day) after it was induced by ethanol. Lipid composition, activity of 5'-nucleotidase (a membrane-associated ectoenzyme) and cytosolic activities of lactate and alcohol dehydrogenases in the plasma membrane of gastric mucosa were determined.Histological studies of gastric samples from the experimental groups were included.RESULTS: Ethanol elicited the histological profile of gastritis characterized by loss of the surface epithelium and infiltration of polymorphonuclear leukocytes.Phosphatidylcholine (PC) decreased and cholesterol content increased in plasma membranes of the gastric mucosa. In addition, cytosolic activity increased while the activity of alcohol dehydrogenases decreased. The administration of mucilage promptly corrected these enzymatic changes. In fact, mucilage readily accelerated restoration of the ethanol-induced histological alterations and the disturbances in plasma membranes of gastric mucosa, showing a univocal anti-inflammatory effect.The activity of 5'-nucleotidase correlated with the changes in lipid composition and the fluidity of gastric mucosal plasma membranes.CONCLUSION: The beneficial action of mucilage seems correlated with stabilization of plasma membranes of damaged gastric mucosa. Molecular interactions between mucilage monosaccharides and membrane phospholipids,mainly PC and phosphatidylethanolamine (PE), may be the relevant features responsible for changing activities of membrane-attached proteins during the healing process after chronic gastric mucosal damage.

  18. Glutamine supplementation attenuates ethanol-induced disruption of apical junctional complexes in colonic epithelium and ameliorates gut barrier dysfunction and fatty liver in mice.

    Chaudhry, Kamaljit K; Shukla, Pradeep K; Mir, Hina; Manda, Bhargavi; Gangwar, Ruchika; Yadav, Nikki; McMullen, Megan; Nagy, Laura E; Rao, RadhaKrishna

    2016-01-01

    Previous in vitro studies showed that glutamine (Gln) prevents acetaldehyde-induced disruption of tight junctions and adherens junctions in Caco-2 cell monolayers and human colonic mucosa. In the present study, we evaluated the effect of Gln supplementation on ethanol-induced gut barrier dysfunction and liver injury in mice in vivo. Ethanol feeding caused a significant increase in inulin permeability in distal colon. Elevated permeability was associated with a redistribution of tight junction and adherens junction proteins and depletion of detergent-insoluble fractions of these proteins, suggesting that ethanol disrupts apical junctional complexes in colonic epithelium and increases paracellular permeability. Ethanol-induced increase in colonic mucosal permeability and disruption of junctional complexes were most severe in mice fed Gln-free diet. Gln supplementation attenuated ethanol-induced mucosal permeability and disruption of tight junctions and adherens junctions in a dose-dependent manner, indicating the potential role of Gln in nutritional intervention to alcoholic tissue injury. Gln supplementation dose-dependently elevated reduced-protein thiols in colon without affecting the level of oxidized-protein thiols. Ethanol feeding depleted reduced protein thiols and elevated oxidized protein thiols. Ethanol-induced protein thiol oxidation was most severe in mice fed with Gln-free diet and absent in mice fed with Gln-supplemented diet, suggesting that antioxidant effect is one of the likely mechanisms involved in Gln-mediated amelioration of ethanol-induced gut barrier dysfunction. Ethanol feeding elevated plasma transaminase and liver triglyceride, which was accompanied by histopathologic lesions in the liver; ethanol-induced liver damage was attenuated by Gln supplementation. These results indicate that Gln supplementation ameliorates alcohol-induced gut and liver injury. PMID:26365579

  19. Chemokines accentuating protumoral activities in oral cancer microenvironment possess an imperious stratagem for therapeutic resolutions.

    Panda, Swagatika; Padhiary, Subrat Kumar; Routray, Samapika

    2016-09-01

    Chemokines, the chemotactic cytokines have established their role in tumorigenesis and tumor progression. Studies, which explored their role in oral cancer for protumoral activity, point towards targeting chemokines for oral squamous cell carcinoma therapy. The need of the hour is to emphasize/divulge in the activities of chemokine ligands and their receptors in the tumor microenvironment for augmentation of such stratagems. This progressing sentience of chemokines and their receptors has inspired this review which is an endeavour to comprehend their role as an aid in accentuating hallmarks of cancer and targeted therapy. PMID:27531867

  20. Protective Effects of Emodin and Chrysophanol Isolated from Marine Fungus Aspergillus sp. on Ethanol-Induced Toxicity in HepG2/CYP2E1 Cells

    Qian, Zhong-Ji; Zhang, Chen; Li, Yong-Xin; Je, Jae-Young; Kim, Se-Kwon; Jung, Won-Kyo

    2011-01-01

    Alcohol-induced liver injury progresses from fatty infiltration followed by a harmful cause of inflammation leading to an irreversible damage. In this study, two compounds (emodin and chrysophanol) isolated from marine fungus Aspergillus sp. were examined for their protective effects against ethanol-induced toxicity in vitro. Ethanol-induced HepG2/CYP2E1 cells were treated with the compounds at various concentrations, and the results showed that there was a dose-dependent decrease of gamma-gl...

  1. Estrogen blocks the protective action of melatonin in a behavioral model of ethanol-induced hangover in mice.

    Karadayian, A G; Mac Laughlin, M A; Cutrera, R A

    2012-09-10

    Melatonin has antioxidant and neuroprotective properties in human beings and experimental models, as well as 'anti-estrogenic' effects. Ethanol (EtOH) affects various behavioral parameters during a period known as ethanol-induced hangover. Our study evaluated the neuroprotective effect of melatonin on motor performance during ethanol hangover in male and female Swiss mice. The females were subjected to specific hormonal states: ovariectomized (OVX) and OVX estrogenized (OVX-E(2)). Mice received melatonin (25 μg/ml) or vehicle in their drinking water for seven days and were given intraperitoneal (i.p.) injections of EtOH (3.8 g/kg) or saline on the morning of the eighth day. Motor performance was evaluated by the tightrope test 6h after EtOH exposure (hangover onset). During ethanol hangover, males exhibited lower motor performance than controls (phangover (phangover led to a better motor performance in OVX compared with intact females (phangover. PMID:22819771

  2. Pyranocycloartobiloxanthone A, a novel gastroprotective compound from Artocarpus obtusus Jarret, against ethanol-induced acute gastric ulcer in vivo.

    Sidahmed, Heyam M A; Hashim, Najihah Mohd; Amir, Junaidah; Abdulla, Mahmood Ameen; Hadi, A Hamid A; Abdelwahab, Siddig Ibrahim; Taha, Manal Mohamed Elhassan; Hassandarvish, Pouya; Teh, Xinsheng; Loke, Mun Fai; Vadivelu, Jamuna; Rahmani, Mawardi; Mohan, Syam

    2013-07-15

    Pyranocycloartobiloxanthone A (PA), a xanthone derived from the Artocarpus obtusus Jarret, belongs to the Moraceae family which is native to the tropical forest of Malaysia. In this study, the efficacy of PA as a gastroprotective compound was examined against ethanol-induced ulcer model in rats. The rats were pretreated with PA and subsequently exposed to acute gastric lesions induced by absolute ethanol. The ulcer index, gastric juice acidity, mucus content, histological analysis, glutathione (GSH) levels, malondialdehyde level (MDA), nitric oxide (NO) and non-protein sulfhydryl group (NP-SH) contents were evaluated in vivo. The activities of PA as anti-Helicobacter pylori, cyclooxygenase-2 (COX-2) inhibitor and free radical scavenger were also investigated in vitro. The results showed that the oral administration of PA protects gastric mucosa from ethanol-induced gastric lesions. PA pretreatment significantly (p<0.05) restored the depleted GSH, NP-SH and NO levels in the gastric homogenate. Moreover, PA significantly (p<0.05) reduced the elevated MDA level due to ethanol administration. The gastroprotective effect of PA was associated with an over expression of HSP70 and suppression of Bax proteins in the ulcerated tissue. In addition, PA exhibited a potent FRAP value and significant COX-2 inhibition. It also showed a significant minimum inhibitory concentration (MIC) against H. pylori bacterium. The efficacy of PA was accomplished safely without the presence of any toxicological parameters. The results of the present study indicate that the gastroprotective effect of PA might contribute to the antioxidant and anti-inflammatory properties as well as the anti-apoptotic mechanism and antibacterial action against Helicobacter pylori. PMID:23570997

  3. Serotoninergic involvement in ethanol-induced alterations of thermoregulation in long-sleep and short-sleep mice.

    French, T A; Weiner, N

    1991-11-01

    The effect of ethanol and pentobarbital on in vivo tryptophan hydroxylase activity and its relationship to drug-induced alterations of thermoregulation was examined in long-sleep (LS) and short-sleep (SS) mice. Serotonin function was measured in both the presence and absence of ethanol or pentobarbital in six discrete brain regions. Differences in basal levels of serotonin, 5-hydroxyindole acetic acid or in vivo tryptophan hydroxylase (TpH) activity were found only in the hypothalamus and dorsal raphe nuclei (SS slightly higher). Ethanol (4.2 g/kg i.p) caused significant reductions in in vivo TpH activity in the dorsal and pontine-medullary raphe nuclei and hypothalamus (putative thermoregulatory areas) in both LS (50-60% decrease) and SS (15-30% decrease) mice, but it had no effect on TpH activity in the striatum, cortex or hippocampus. The greater degree of ethanol-induced reduction in TpH activity in LS mice was associated with a greater degree of hypothermia (LS, 4.2 degrees C vs SS, 2.0 degrees C). Pentobarbital had equivalent effects in LS and SS mice on TpH activity in central nervous system thermoregulatory areas (decreases of 40-60%) and on body temperature (decreases of 6.8-7.5 degrees C). When the mice were given ethanol at an elevated environmental temperature (34 degrees C) the hypothermia was almost abolished completely, but depressant effects on TpH activity remained, suggesting that ethanol-induced decreases in TpH activity were direct effects and not secondary to hypothermia. Alterations in ethanol or pentobarbital elimination did not appear to account for the observed differences.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:1941631

  4. Biochemical and immunological basis of silymarin effect, a milk thistle (Silybum marianum) against ethanol-induced oxidative damage.

    Das, Subir Kumar; Mukherjee, Sukhes

    2012-06-01

    Ethanol metabolism induces generation of excessive amount of reactive oxygen species (ROS) which results in immune dysfunction. We examined the efficacy of silymarin on ethanol-induced oxidative stress, immunomodulatory activity, and vascular function in mice blood. Effectiveness of silymarin was compared with potent antioxidant ascorbic acid. In the present study, 8- to 10-week-old male BALB/c mice (20-30 g) were divided into the four groups of six each. One group were fed with ethanol (1.6 g/kg body weight), while second group were fed with ethanol (1.6 g/kg body weight) and silybin (250 mg/kg body weight), and the third group were exposed to ethanol (250 mg/kg body weight) and ascorbic acid (250 mg/kg body weight) per day for 12 weeks. The control group was fed with isocaloric glucose solution instead of ethanol. Ethanol exposure significantly increased thiobarbituric acid reactive substance (TBARS) and nitrite levels besides glutathione-S-transferase (GST) activity, and significantly decreased reduced glutathione (GSH) content and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and glutathione peroxidase (GPx) in whole blood hemolyzate, while silymarin treatment significantly normalized these altered parameters. Silymarin significantly prevented ethanol-induced, elevated activities of interleukin (IL)-10, tumor necrosis factor (TNF)-α, γ interferon (IFN-γ), vascular endothelial growth factor (VEGF)-A, and transforming growth factor (TGF)-β1, as well as decreased IL-4 activity in mice blood. These results were comparable with the activity of ascorbic acid. PMID:22409310

  5. PROGRAM OF RECREATIONAL AND HEALTH ACTIVITIES FOR ADOLESCENTS WITH CHARACTER'S ACCENTUATIONS

    Vorobiova A.V.

    2012-07-01

    Full Text Available The problem of using psychosomatic approach for correction the behavior of adolescents with character's accentuations was considered. The author's program of recreational and health activities for adolescents was grounded and offered, taking into account the level of social adaptation and psychological features of character. The researches were conducted on the basis of secondary schools № 5, 7, 11 of the Romny town, Sumy region with 12-16 years old teens (n=412, including 218 girls and 194 boys. It is determined that psychosomatic approach in health and recreation program provides for the development and planning means and methods that influence not only on the level of somatic and physical health, but also on the structure of adolescents' personality. It is recommended the author's program, that consists of three stages and solved the three groups of problems: health, training and educational, was developed and inculcated in an educational process.

  6. TREM-1-accentuated lung injury via miR-155 is inhibited by LP17 nanomedicine.

    Yuan, Zhihong; Syed, Mansoor; Panchal, Dipti; Joo, Myungsoo; Bedi, Chetna; Lim, Sokbee; Onyuksel, Hayat; Rubinstein, Israel; Colonna, Marco; Sadikot, Ruxana T

    2016-03-01

    Triggering receptors expressed on myeloid cell-1 (TREM-1) is a superimmunoglobulin receptor expressed on myeloid cells. Synergy between TREM-1 and Toll-like receptor amplifies the inflammatory response; however, the mechanisms by which TREM-1 accentuates inflammation are not fully understood. In this study, we investigated the role of TREM-1 in a model of LPS-induced lung injury and neutrophilic inflammation. We show that TREM-1 is induced in lungs of mice with LPS-induced acute neutrophilic inflammation. TREM-1 knockout mice showed an improved survival after lethal doses of LPS with an attenuated inflammatory response in the lungs. Deletion of TREM-1 gene resulted in significantly reduced neutrophils and proinflammatory cytokines and chemokines, particularly IL-1β, TNF-α, and IL-6. Physiologically deletion of TREM-1 conferred an immunometabolic advantage with low oxygen consumption rate (OCR) sparing the respiratory capacity of macrophages challenged with LPS. Furthermore, we show that TREM-1 deletion results in significant attenuation of expression of miR-155 in macrophages and lungs of mice treated with LPS. Experiments with antagomir-155 confirmed that TREM-1-mediated changes were indeed dependent on miR-155 and are mediated by downregulation of suppressor of cytokine signaling-1 (SOCS-1) a key miR-155 target. These data for the first time show that TREM-1 accentuates inflammatory response by inducing the expression of miR-155 in macrophages and suggest a novel mechanism by which TREM-1 signaling contributes to lung injury. Inhibition of TREM-1 using a nanomicellar approach resulted in ablation of neutrophilic inflammation suggesting that TREM-1 inhibition is a potential therapeutic target for neutrophilic lung inflammation and acute respiratory distress syndrome (ARDS). PMID:26684249

  7. Alterations in ethanol-induced behaviors and consumption in knock-in mice expressing ethanol-resistant NMDA receptors.

    Carolina R den Hartog

    Full Text Available Ethanol's action on the brain likely reflects altered function of key ion channels such as glutamatergic N-methyl-D-aspartate receptors (NMDARs. In this study, we determined how expression of a mutant GluN1 subunit (F639A that reduces ethanol inhibition of NMDARs affects ethanol-induced behaviors in mice. Mice homozygous for the F639A allele died prematurely while heterozygous knock-in mice grew and bred normally. Ethanol (44 mM; ∼0.2 g/dl significantly inhibited NMDA-mediated EPSCs in wild-type mice but had little effect on responses in knock-in mice. Knock-in mice had normal expression of GluN1 and GluN2B protein across different brain regions and a small reduction in levels of GluN2A in medial prefrontal cortex. Ethanol (0.75-2.0 g/kg; i.p. increased locomotor activity in wild-type mice but had no effect on knock-in mice while MK-801 enhanced activity to the same extent in both groups. Ethanol (2.0 g/kg reduced rotarod performance equally in both groups but knock-in mice recovered faster following a higher dose (2.5 g/kg. In the elevated zero maze, knock-in mice had a blunted anxiolytic response to ethanol (1.25 g/kg as compared to wild-type animals. No differences were noted between wild-type and knock-in mice for ethanol-induced loss of righting reflex, sleep time, hypothermia or ethanol metabolism. Knock-in mice consumed less ethanol than wild-type mice during daily limited-access sessions but drank more in an intermittent 24 h access paradigm with no change in taste reactivity or conditioned taste aversion. Overall, these data support the hypothesis that NMDA receptors are important in regulating a specific constellation of effects following exposure to ethanol.

  8. Acute toxicity and gastroprotective role of M. pruriens in ethanol-induced gastric mucosal injuries in rats.

    Golbabapour, Shahram; Hajrezaie, Maryam; Hassandarvish, Pouya; Abdul Majid, Nazia; Hadi, A Hamid A; Nordin, Noraziah; Abdulla, Mahmood A

    2013-01-01

    The investigation was to evaluate gastroprotective effects of ethanolic extract of M. pruriens leaves on ethanol-induced gastric mucosal injuries in rats. Forty-eight rats were divided into 8 groups: negative control, extract control, ulcer control, reference control, and four experimental groups. As a pretreatment, the negative control and the ulcer control groups were orally administered carboxymethylcellulose (CMC). The reference control was administered omeprazole orally (20 mg/kg). The ethanolic extract of M. pruriens leaves was given orally to the extract control group (500 mg/kg) and the experimental groups (62.5, 125, 250, and 500 mg/kg). After 1 h, CMC was given orally to the negative and the extract control groups. The other groups received absolute ethanol. The rats were sacrificed after 1 h. The ulcer control group exhibited significant mucosal injuries with decreased gastric wall mucus and severe damage to the gastric mucosa. The extract caused upregulation of Hsp70 protein, downregulation of Bax protein, and intense periodic acid schiff uptake of glandular portion of stomach. Gastric mucosal homogenate showed significant antioxidant properties with increase in synthesis of PGE2, while MDA was significantly decreased. The ethanolic extract of M. pruriens leaves was nontoxic (<5 g/kg) and could enhance defensive mechanisms against hemorrhagic mucosal lesions. PMID:23781513

  9. Antioxidant Properties and Gastroprotective Effects of 2-(EthylthioBenzohydrazones on Ethanol-Induced Acute Gastric Mucosal Lesions in Rats.

    Nafal Nazarbahjat

    Full Text Available A series of new 2-(ethylthiobenzohydrazone derivatives (1-6 were prepared and characterised by IR, 1H NMR, and 13C NMR spectroscopy and mass spectrometry. The newly prepared compounds were screened for their in vitro antioxidant activities using free radical scavenging 2,2-diphenyl-1-picrylhydrazyl (DPPH and ferric reducing antioxidant power (FRAP assays. Among them, most powerful antioxidant, compound 1 has been selected in order to illustrate anti-ulcer effect on ethanol-induced gastric mucosal lesions in rats. Four groups of Sprague Dawley rats were respectively treated with 10% Tween 20 as ulcer control group, 20 mg/kg omeprazole as reference group, 50 mg/kg and 100 mg/kg compound 1 as experimental animals. Macroscopically, ulcer control group showed extensive hemorrhagic lesions of gastric mucosa compared with omeprazole or compound 1. Rats pre-treated with compound 1 showed increased in gastric pH and gastric mucus. Histologically, ulcer control group showed severe damage to gastric mucosa with edema and leucocytes infiltration of submucosal layer. In immunohistochemical analysis, rats which were pre-treated with compound 1 showed up-regulation of HSP70 and down-regulation of Bax proteins. In conclusion, the gastroprotective effect of compound 1 may be due to its antioxidant activity, and/or due to up-regulation of HSP70 and down-regulation of Bax protein in stained tissue section.

  10. Protective effect of Solanum nigrum fruit extract on the functional status of liver and kidney against ethanol induced toxicity

    Mirunalini Sankaran

    2012-04-01

    Full Text Available The trend in using natural products has increased and the active plant extracts are frequently screened for new drug discoveries. The present study was aimed to investigate the effect of Solanum nigrum fruit extract (SNFEt on ethanol induced toxicity in rats. Male albino wistar rats were intoxicated with ethanol and the effect of SNFEt on the levels of hepatic marker enzymes (aspartate aminotransferase (AST, alanine aminotransferase (ALT, alkaline phosphatase (ALP, gamma glutamyl transferase (GGT and bilirubin, renal markers (urea, uric acid and creatinine and antioxidant status such as Superoxide dismutase (SOD, catalase (CAT, glutathione peroxidase (GPx, reduced glutathione (GSH were assessed in liver and kidney.  Ethanol intoxicated rats showed significant rise in hepatic marker enzymes, renal markers where the antioxidant status were found to be decreased. Supplementation of SNFEt altered these changes to near normal which was also compared with the standard drug silymarin. This beneficial activity of the extract might be considered as an adjuvant drug in the treatment of liver disorders. Thus we propose that dietary intake of Solanum nigrum fruits offers protection against toxicity.

  11. Cinitapride protects against ethanol-induced gastric mucosal injury in rats: role of 5-hydroxytryptamine, prostaglandins and sulfhydryl compounds.

    Alarcón-de-la-Lastra Romero, C; López, A; Martín, M J; la Casa, C; Motilva, V

    1997-04-01

    This study was designed to determine the gastroprotective properties of cinitapride (CNT), a novel prokinetic benzamide derivative agonist of 5-HT4 and 5-HT1 receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol. Results were compared with those for 5-hydroxytryptamine (5-HT: 10 mg kg-1). The possible involvements of gastric mucus secretion, endogenous prostaglandins (PGs) and sulfhydryl compounds (SH) in the protection mediated by CNT were also examined. Intraperitoneal administration of CNT (0.50 and 1 mg kg-1), 30 min before ethanol, significantly prevented gastric ulceration and increased the hexosamine content of gastric mucus. CNT (1 mg kg-1) also produced a significant increase in gastric mucosal levels of PGE2, but did not induce any significant changes in SH values. On the contrary, pretreatment with 5-HT worsened ethanol-induced erosions, however, did not affect gastric mucus secretion, glycoprotein content or PGE2 levels, although the non-protein SH fraction was significantly decreased. The present results demonstrate that the gastroprotective effects of CNT could be partly explained by a complex PG dependent mechanism. We suggest that 5-HT dependent mechanisms through 5-HT2 receptor blockade and 5-HT1 receptor activation could be also involved. PMID:9211565

  12. Protective Effect of Areca catechu Leaf Ethanol Extract Against Ethanol-Induced Gastric Ulcers in ICR Mice.

    Lee, Kang Pa; Choi, Nan Hee; Sudjarwo, Giftania Wardani; Ahn, Sang-Hyun; Park, In-Sik; Lee, Sang-Rak; Hong, Heeok

    2016-02-01

    Gastric ulcer is a common digestive disorder that results in considerable suffering. Hence, this digestive pathology has been the focus of a number of recent studies. Although numerous drugs have been developed to treat gastric ulcers, therapeutic approaches for many of the complications associated with these drugs remain to be identified. For this reason, many natural compounds have been explored as alternatives for these drugs. In this study, we have investigated the effectiveness of Areca catechu leaf ethanol extract (ACE) for treating ethanol-induced gastric ulcers in mice. We performed histological as well as immunohistochemical examinations to explore the therapeutic properties of ACE. We also examined the levels of inflammatory signaling molecules to confirm the anti-inflammatory effects of ACE. The histochemical data demonstrate that ACE can protect the mucosal epithelium as well as the vascular supply in the gastric tract. Furthermore, ACE significantly reduced the expression levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 receptor (IL-6R), inducible NO synthase (iNOS), cyclooxygenase 2 (COX2), and nuclear factor-kappa B (NF-κB). Taken together, these data suggest that ACE administration may have the potential as an alternative treatment for gastric ulcer because of its cytoprotective and anti-inflammatory effects and ability to promote the rejuvenation and revascularization of the damaged gastric epithelium. PMID:26540449

  13. Acute Toxicity and Gastroprotective Role of M. pruriens in Ethanol-Induced Gastric Mucosal Injuries in Rats

    Hassandarvish, Pouya; Abdul Majid, Nazia; Hadi, A. Hamid A.; Nordin, Noraziah; Abdulla, Mahmood A.

    2013-01-01

    The investigation was to evaluate gastroprotective effects of ethanolic extract of M. pruriens leaves on ethanol-induced gastric mucosal injuries in rats. Forty-eight rats were divided into 8 groups: negative control, extract control, ulcer control, reference control, and four experimental groups. As a pretreatment, the negative control and the ulcer control groups were orally administered carboxymethylcellulose (CMC). The reference control was administered omeprazole orally (20 mg/kg). The ethanolic extract of M. pruriens leaves was given orally to the extract control group (500 mg/kg) and the experimental groups (62.5, 125, 250, and 500 mg/kg). After 1 h, CMC was given orally to the negative and the extract control groups. The other groups received absolute ethanol. The rats were sacrificed after 1 h. The ulcer control group exhibited significant mucosal injuries with decreased gastric wall mucus and severe damage to the gastric mucosa. The extract caused upregulation of Hsp70 protein, downregulation of Bax protein, and intense periodic acid schiff uptake of glandular portion of stomach. Gastric mucosal homogenate showed significant antioxidant properties with increase in synthesis of PGE2, while MDA was significantly decreased. The ethanolic extract of M. pruriens leaves was nontoxic (<5 g/kg) and could enhance defensive mechanisms against hemorrhagic mucosal lesions. PMID:23781513

  14. Apium graveolens accentuates urinary Ca +2 excretions in experimental model of nephrocalcinosis

    Faruk H Al Jawad

    2011-01-01

    Full Text Available Nephrocalcinosis (NC is a state characterised by deposition of calcium phosphate or oxalate in the renal parenchyma due to different clinical conditions. Apium graveolens (Celery is a popular vegetable added to salads and many cooked dishes, used in Chinese medicine to reduce high blood pressure and in Arabic medicine to relieve renal pains. To evaluate the effect of A. graveolens in reducing calcium deposits from renal parenchyma in rabbit models with induced NC by a large dose of oxalic acid. A. graveolens produced a significant reduction of blood urea nitrogen (5.7±0.05 vs 7.3±0.2 mmol/l, serum creatinine (87.2±0.63 vs 97.3±0.5 mmol/l and serum Na + levels (136.8±0.2 vs 142.16±0.7 mmol/l with non-significant reduction in serum K + (3.3±0.8 vs 3.8±0.03. There is a significant reduction in calcium deposition in renal parenchyma in comparison to the control group after ten days of treatment. A. graveolens showed a significant diuretic effect that accentuates the excretion of urinary calcium.

  15. A Role for Ethanol-Induced Oxidative Stress in Controlling Lineage Commitment of Mesenchymal Stromal Cells Through Inhibition of Wnt/β-Catenin Signaling

    Chen, Jin-Ran; Lazarenko, Oxana P.; Shankar, Kartik; Blackburn, Michael L; Badger, Thomas M.; Ronis, Martin J.

    2009-01-01

    The mechanisms by which chronic ethanol intake induces bone loss remain unclear. In females, the skeletal response to ethanol varies depending on physiologic status (e.g., cycling, pregnancy, or lactation). Ethanol-induced oxidative stress appears to be a key event leading to skeletal toxicity. In this study, ethanol-containing liquid diets were fed to postlactational female Sprague-Dawley rats intragastrically for 4 weeks beginning at weaning. Ethanol consumption decreased bone mineral densi...

  16. Anti-Ulcerogenic Properties of Lycium chinense Mill Extracts against Ethanol-Induced Acute Gastric Lesion in Animal Models and Its Active Constituents

    Opeyemi J. Olatunji; Hongxia Chen; Yifeng Zhou

    2015-01-01

    The objective of this study was to explore the gastroprotective properties of the aerial part of Lycium chinense Mill (LCA) against ethanol-induced gastric mucosa lesions in mice models. Administration of LCA at doses of 50, 100, 200 and 400 mg/kg body weight prior to ethanol consumption dose dependently inhibited gastric ulcers. The gastric mucosal injury was analyzed by gastric juice acidity, glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO) activit...

  17. Sex differences in the effects of ethanol pre-exposure during adolescence on ethanol-induced conditioned taste aversion in adult rats

    Sherrill, Luke K.; Berthold, Claire; Koss, Wendy A.; Juraska, Janice M.; Gulley, Joshua M.

    2011-01-01

    Alcohol use, which typically begins during adolescence and differs between males and females, is influenced by both the rewarding and aversive properties of the drug. One way adolescent alcohol use may modulate later consumption is by reducing alcohol s aversive properties. Here, we used a conditioned taste aversion (CTA) paradigm to determine if pre-exposure to alcohol (ethanol) during adolescence would attenuate ethanol-induced CTA assessed in adulthood in a sex-dependent manner. Male and f...

  18. Myocardial contractility

    Comet, M.; Machecourt, J.

    1988-01-01

    The myocardial contractility characterizes the intensity of the activation representing the globality of the processes which lead to the formation of the sites where the strength is generated. Some parameters allowing a quantification of the contractility are measured during the isovolumic phase of the ventricular contraction: they are essentially dP/dt/sub max/, and eventually V/sub max/. For the measurement of these parameters, a pressure detector needs to be introduced into the left ventricle. Other parameters are measured during the systolic ejection phase: they are the ejection fraction, which is easy to measure and is very load dependant, and the maximal elastance. This last parameter is not easy to measure, but seems load independant. With the radioisotopes, it is possible to measure the ejection fraction and the maximal elastance. Contractility measurements are of interest in the study of ischemic cardiopathies and of valvular desease.

  19. Protective and therapeutic effects of an extract mixture of alder tree, labiate herb, milk thistle green bean-rice bran fermentation, and turnip against ethanol-induced toxicity in the rat

    Baek, Min-Won; Seok, Seung-Hyeok; Lee, Hui-Young; Kim, Dong Jae; Lee, Byoung-Hee; Ahn, Young-Tae; Lim, Kwang-Sei; Huh, Chul-Sung; Park, Jae-Hak

    2008-01-01

    An herbal extract mixture and yogurt added to the herbal extract mixture were tested for their protective and therapeutic effects on ethanol-induced liver injury. The herbal extract mixture, yogurt and commercial drugs were used for treatment for two weeks prior to administering a single oral dose of ethanol (3 g/kg body weight). The herbal extract mixture and yogurt added to the herbal extract mixture were found to provide protection against ethanol-induced toxicity comparable to the commerc...

  20. In vivo antioxidant and antiulcer activity of Parkia speciosa ethanolic leaf extract against ethanol-induced gastric ulcer in rats.

    Rami Al Batran

    Full Text Available BACKGROUND: The current study was carried out to examine the gastroprotective effects of Parkia speciosa against ethanol-induced gastric mucosa injury in rats. METHODOLOGY/PRINCIPAL FINDINGS: Sprague Dawley rats were separated into 7 groups. Groups 1-2 were orally challenged with carboxymethylcellulose (CMC; group 3 received 20 mg/kg omeprazole and groups 4-7 received 50, 100, 200 and 400 mg/kg of ethanolic leaf extract, respectively. After 1 h, CMC or absolute ethanol was given orally to groups 2-7. The rats were sacrificed after 1 h. Then, the injuries to the gastric mucosa were estimated through assessment of the gastric wall mucus, the gross appearance of ulcer areas, histology, immunohistochemistry and enzymatic assays. Group 2 exhibited significant mucosal injuries, with reduced gastric wall mucus and severe damage to the gastric mucosa, whereas reductions in mucosal injury were observed for groups 4-7. Groups 3-7 demonstrated a reversal in the decrease in Periodic acid-Schiff (PAS staining induced by ethanol. No symptoms of toxicity or death were observed during the acute toxicity tests. CONCLUSION: Treatment with the extract led to the upregulation of heat-shock protein 70 (HSP70 and the downregulation of the pro-apoptotic protein BAX. Significant increases in the levels of the antioxidant defense enzymes glutathione (GSH and superoxide dismutase (SOD in the gastric mucosal homogenate were observed, whereas that of a lipid peroxidation marker (MDA was significantly decreased. Significance was defined as p<0.05 compared to the ulcer control group (Group 2.

  1. Hepatoprotective potential of Lavandula coronopifolia extracts against ethanol induced oxidative stress-mediated cytotoxicity in HepG2 cells.

    Farshori, Nida Nayyar; Al-Sheddi, Ebtsam S; Al-Oqail, Mai M; Hassan, Wafaa H B; Al-Khedhairy, Abdulaziz A; Musarrat, Javed; Siddiqui, Maqsood A

    2015-08-01

    The present investigations were carried out to study the protective potential of four extracts (namely petroleum ether extract (LCR), chloroform extract (LCM), ethyl acetate extract (LCE), and alcoholic extract (LCL)) of Lavandula coronopifolia on oxidative stress-mediated cell death induced by ethanol, a known hepatotoxin in human hapatocellular carcinoma (HepG2) cells. Cells were pretreated with LCR, LCM, LCE, and LCL extracts (10-50 μg/ml) of L. coronopifolia for 24 h and then ethanol was added and incubated further for 24 h. After the exposure, cell viability using (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and neutral red uptake assays and morphological changes in HepG2 cells were studied. Pretreatment with various extracts of L. coronpifolia was found to be significantly effective in countering the cytotoxic responses of ethanol. Antioxidant properties of these L. coronopifolia extracts against reactive oxygen species (ROS) generation, lipid peroxidation (LPO), and glutathione (GSH) levels induced by ethanol were investigated. Results show that pretreatment with these extracts for 24 h significantly inhibited ROS generation and LPO induced and increased the GSH levels reduced by ethanol. The data from the study suggests that LCR, LCM, LCE, and LCL extracts of L. coronopifolia showed hepatoprotective activity against ethanol-induced damage in HepG2 cells. However, a comparative study revealed that the LCE extract was found to be the most effective and LCL the least effective. The hepatoprotective effects observed in the study could be associated with the antioxidant properties of these extracts of L. coronopifolia. PMID:23546397

  2. Tectoridin, an isoflavone glycoside from the flower of Pueraria lobata, prevents acute ethanol-induced liver steatosis in mice

    In traditional Chinese medicine, the flower of Pueraria lobata (Puerariae Flos) has been used in therapy to counteract the problems associated with alcohol drinking and liver injury. In this study, we investigated the hepatoprotective effects and its mechanisms of tectoridin, an isoflavone glycoside from the flower of P. lobata (Willd.) Ohwi. Ethanol (5 g/kg) was given orally every 12 h for a total of three doses. 1 h after the last dose of ethanol, tectoridin (25, 50 and 100 mg/kg) was given intragastrically five times in three consecutive days. The mice were sacrificed at 4 h after tectoridin treatment. Peroxisome proliferators-activated receptor α (PPARα), sterol regulatory element-binding protein (SREBP)-1c and their target genes were evaluated by biochemical analysis and quantitative real-time polymerase chain reaction (qPCR). Mitochondria were isolated for the mitochondrial permeability transition (MPT) and membrane potential (ΔΨm) assay. Acute ethanol exposure resulted in the significant increase of the alanine aminotransferase (ALT), aspartate aminotransferase (AST) and triglyceride (TG) levels and hepatic mitochondria dysfunction shown as the increase of MPT and the decrease of ΔΨm. However, tectoridin treatment dramatically attenuated these effects. In addition, tectoridin remarkably alleviated the over-production of thiobarbituric acid-reactive substance. Furthermore, tectoridin inhibited the decrease of PPARα expression and its target genes, including medium-chain acyl-CoA dehydrogenase (MCAD), acyl-CoA oxidase (ACO) and cytochrome P450 4A (CYP 4A) at mRNA and enzyme activity levels. These data showed that tectoridin protected against ethanol-induced liver steatosis mainly through modulating the disturbance of PPARα pathway and ameliorating mitochondrial function.

  3. Fas Regulates Macrophage Polarization and Fibrogenic Phenotype in a Model of Chronic Ethanol-Induced Hepatocellular Injury.

    Isayama, Fuyumi; Moore, Sherri; Hines, Ian N; Wheeler, Michael D

    2016-06-01

    The role of Fas-mediated apoptosis and its effect on proinflammatory cytokine production in early alcoholic liver disease has not been addressed. Wild-type mice (C57Bl/6) or mice with a functional mutation in the Fas ligand (B6.gld) were given either high-fat control diet or ethanol diet by intragastric cannulation for 2 or 4 weeks. Liver injury, hepatic lipid accumulation, and proinflammatory cytokine production associated with chronic ethanol consumption were largely prevented in B6.gld mice compared with wild-type mice. Conversely, B6.gld mice given ethanol exhibited increases in collagen deposition, hepatic collagen gene expression, and profibrogenic cytokines (eg, transforming growth factor-β and IL-13) and alterations in matrix remodeling proteins (eg, matrix metalloproteinases and tissue inhibitor of metalloproteinases) compared with wild-type mice. Hepatic F4/80(+) macrophage populations were increased significantly in B6.gld mice compared with wild-type mice; hepatic CD3(+) cell populations were not significantly different. Importantly, a shift toward the expression of M2/Th2 cytokines (eg, IL-4 and IL-13) after ethanol exposure was observed in B6.gld mice compared with classical M1 cytokine expression in wild-type mice under similar conditions. In isolated macrophages, stimulation of Fas receptor minimally enhances lipopolysaccharide-induced M1 cytokine production and significantly limits M2 cytokine production. These data support the hypothesis that Fas-mediated signaling is important for an early ethanol-induced proinflammatory response but limits the profibrogenic response, regulating collagen production in response to chronic ethanol. PMID:27102767

  4. Anti-ulcerogenic effect of cavidine against ethanol-induced acute gastric ulcer in mice and possible underlying mechanism.

    Li, Weifeng; Wang, Xiumei; Zhang, Hailin; He, Zehong; Zhi, Wenbing; Liu, Fang; Wang, Yu; Niu, Xiaofeng

    2016-09-01

    Cavidine, a major alkaloid compound isolated from Corydalis impatiens, has various pharmacological effects but its effect on gastric ulcer has not been previously explored. The current study aimed to investigate the possible anti-ulcerogenic potential of cavidine in the model of ethanol-induced gastric ulcer. Mice received cavidine (1, 5 or 10mg/kg, ig), cimetidine (CMD, 100mg/kg, ig) or vehicle at 12h and 1h before absolute ethanol administration (0.5mL/100g), and animals were euthanized 3h after ethanol ingestion. Gross and histological gastric lesions, biochemical, immunological and Western blot parameters were taken into consideration. The results showed that ethanol administration produced apparent mucosal injuries with morphological and histological damage, whereas cavidine pre-treatment reduced the gastric injuries. Cavidine pre-treatment also ameliorated the contents of malonaldehyde (MDA) and myeloperoxidase (MPO) activity, and increased the mucosa levels of glutathione (GSH), superoxide dismutase (SOD) and prostaglandin E2 (PGE2), relative to the model group. Also cavidine was able to decrease the levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), inhibit the up-regulation of cyclo-oxygenase-2 (COX-2) expression and activation of Nuclear factor-kappa B (NF-κB) pathway. Taken together, these results indicated that cavidine exerts a gastroprotective effect against gastric ulceration, and the underlying mechanism might be associated with the stimulation of PGE2, reduction of oxidative stress, suppression of NF-κB expression and subsequent reduced COX-2 and pro-inflammatory cytokines. PMID:27380619

  5. Ethanol-induced analgesia

    Pohorecky, L.A.; Shah, P.

    1987-09-07

    The effect of ethanol (ET) on nociceptive sensitivity was evaluated using a new tail deflection response (TDR) method. The IP injection of ET (0.5 - 1.5 g/kg) produced raid dose-dependent analgesia. Near maximal effect (97% decrease in TDR) was produced with the 1.5 g/kg dose of ET ten minutes after injection. At ninety minutes post-injection there was still significant analgesia. Depression of ET-induced nociceptive sensitivity was partially reversed by a 1 mg/kg dose of naloxone. On the other hand, morphine (0.5 or 5.0 mg/kg IP) did not modify ET-induced analgesia, while 3.0 minutes of cold water swim (known to produce non-opioid mediated analgesia) potentiated ET-induced analgesic effect. The 0.5 g/kg dose of ET by itself did not depress motor activity in an open field test, but prevented partially the depression in motor activity produced by cold water swim (CWS). Thus, the potentiation by ET of the depression of the TDR produced by CWS cannot be ascribed to the depressant effects of ET on motor activity. 21 references, 4 figures, 1 table.

  6. Classification of myocardial infarction

    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 and...

  7. Transient myocardial ischemia after myocardial infarction

    Mickley, H

    1995-01-01

    Ambulatory ST-segment monitoring is a relatively new device in the evaluation of myocardial ischemia. The method is unique in allowing us to continuously examine the patient over an extended period of time in a changing environmental milieu. In survivors of acute myocardial infarction the...... prevalence of ambulatory or transient myocardial ischemia is lower than in patients with chronic, stable coronary artery disease. A greater proportion of ischemic episodes, however, are silent than in other subgroups with ischemic heart disease. Early after the infarction, transient myocardial ischemia...... exhibits a circadian variation with a peak activity occurring in the late evening hours. Patients with non-Q wave infarction have more transient myocardial ischemia, whereas thrombolytic therapy seems to result in less residual ischemia. Exercise testing is more sensitive than ambulatory monitoring in the...

  8. Metabolic basis of ethanol-induced cytotoxicity in recombinant HepG2 cells: Role of nonoxidative metabolism

    Chronic alcohol abuse, a major health problem, causes liver and pancreatic diseases and is known to impair hepatic alcohol dehydrogenase (ADH). Hepatic ADH-catalyzed oxidation of ethanol is a major pathway for the ethanol disposition in the body. Hepatic microsomal cytochrome P450 (CYP2E1), induced in chronic alcohol abuse, is also reported to oxidize ethanol. However, impaired hepatic ADH activity in a rat model is known to facilitate a nonoxidative metabolism resulting in formation of nonoxidative metabolites of ethanol such as fatty acid ethyl esters (FAEEs) via a nonoxidative pathway catalyzed by FAEE synthase. Therefore, the metabolic basis of ethanol-induced cytotoxicity was determined in HepG2 cells and recombinant HepG2 cells transfected with ADH (VA-13), CYP2E1 (E47) or ADH + CYP2E1 (VL-17A). Western blot analysis shows ADH deficiency in HepG2 and E47 cells, compared to ADH-overexpressed VA-13 and VL-17A cells. Attached HepG2 cells and the recombinant cells were incubated with ethanol, and nonoxidative metabolism of ethanol was determined by measuring the formation of FAEEs. Significantly higher levels of FAEEs were synthesized in HepG2 and E47 cells than in VA-13 and VL-17A cells at all concentrations of ethanol (100-800 mg%) incubated for 6 h (optimal time for the synthesis of FAEEs) in cell culture. These results suggest that ADH-catalyzed oxidative metabolism of ethanol is the major mechanism of its disposition, regardless of CYP2E1 overexpression. On the other hand, diminished ADH activity facilitates nonoxidative metabolism of ethanol to FAEEs as found in E47 cells, regardless of CYP2E1 overexpression. Therefore, CYP2E1-mediated oxidation of ethanol could be a minor mechanism of ethanol disposition. Further studies conducted only in HepG2 and VA-13 cells showed lower ethanol disposition and ATP concentration and higher accumulation of neutral lipids and cytotoxicity (apoptosis) in HepG2 cells than in VA-13 cells. The apoptosis observed in HepG2 vs

  9. Evaluation of cell proliferation, apoptosis, and dna-repair genes as potential biomarkers for ethanol-induced cns alterations

    Hicks Steven D

    2012-10-01

    Full Text Available Abstract Background Alcohol use disorders (AUDs lead to alterations in central nervous system (CNS architecture along with impaired learning and memory. Previous work from our group and that of others suggests that one mechanism underlying these changes is alteration of cell proliferation, apoptosis, and DNA-repair in neural stem cells (NSCs produced as a consequence of ethanol-induced effects on the expression of genes related to p53-signaling. This study tests the hypothesis that changes in the expression of p53-signaling genes represent biomarkers of ethanol abuse which can be identified in the peripheral blood of rat drinking models and human AUD subjects and posits that specific changes may be correlated with differences in neuropsychological measures and CNS structure. Results Remarkably, microarray analysis of 350 genes related to p53-signaling in peripheral blood leukocytes (PBLs of binge-drinking rats revealed 190 genes that were significantly altered after correcting for multiple testing. Moreover, 40 of these genes overlapped with those that we had previously observed to be changed in ethanol-exposed mouse NSCs. Expression changes in nine of these genes were tested for independent confirmation by a custom QuantiGene Plex (QGP assay for a subset of p53-signaling genes, where a consistent trend for decreased expression of mitosis-related genes was observed. One mitosis-related gene (Pttg1 was also changed in human lymphoblasts cultured with ethanol. In PBLs of human AUD subjects seven p53-signaling genes were changed compared with non-drinking controls. Correlation and principal components analysis were then used to identify significant relationships between the expression of these seven genes and a set of medical, demographic, neuropsychological and neuroimaging measures that distinguished AUD and control subjects. Two genes (Ercc1 and Mcm5 showed a highly significant correlation with AUD-induced decreases in the volume of the left

  10. Perillyl alcohol protects against ethanol induced acute liver injury in Wistar rats by inhibiting oxidative stress, NFκ-B activation and proinflammatory cytokine production

    Oxidative stress and inflammation are two major etiological factors that are suggested to play key roles in the development of ethanol induced liver injury. Release of proinflammatory cytokine like tumor necrosis factor alpha (TNF-α) and activation of nuclear factor kappa-B (NFκ-B) may strongly intensify inflammation and cell damage. Additionally, reactive oxygen species (ROS) also exerts significant effect in this whole cell signaling machinery. The present study was designed to investigate the protective effects of perillyl alcohol (POH) on ethanol-induced acute liver injury in Wistar rats and its probable mechanism. We have successfully demonstrated that pre-treatment with POH, besides exerting antioxidant activity might be able to modulate TNF-α release and NFκ-B activation. Rats were divided into five groups and treated with ethanol or POH via an intragastric tube for one week. Control group was treated with vehicle, and ethanol treated group was given ethanol (5 g/kg body wt). Animal of treatment groups were pretreated with POH (50 and 100 mg/kg body wt) and have been given ethanol. Serum aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase and hepatic malondialdehyde were increased significantly by ethanol treatment. Ethanol administration decreased hepatic reduced glutathione content and various antioxidant enzymes activity. TNF-α production and NFκ-B activation was also found to be increased after ethanol administration. POH pre-treatment significantly ameliorates ethanol induced acute liver injury possibly by inhibition of lipid peroxidation, replenishment of endogenous enzymatic and non-enzymatic defense system, downregulation of TNF-α as well as NFκ-B.

  11. S-adenosyl-methionine decreases ethanol-induced apoptosis in primary hepatocyte cultures by a c-Jun N-terminal kinase activity-independent mechanism

    María del Pilar Cabrales-Romero; Lucrecia Márquez-Rosado; Samia Fattel-Fazenda; Cristina Trejo-Solís; Evelia Arce-Popoca; Leticia Alemén-Lazarini; Saúl Villa-Trevi(n)o

    2006-01-01

    AIM: To determine the role of c-Jun N-terminal kinase (JNK) activity in ethanol-induced apoptosis and the modulation of this signaling cascade by S-Adenosylmethionine (AdoMet).METHODS: Primary hepatocyte cultures were pretreated with 100 μmol/L SP600125, a selective JNK inhibitor, 1 mL/L DMSO or 4 mmol/L AdoMet and then exposed to 100 mmo/L ethanol. Hepatocyte apoptosis was determined by the TUNEL and DNA ladder assays.JNK activity and its inhibition by SP600125 and AdoMet were determined by Western blot analysis of c-jun phosphorylation and Bid fragmentation. SP600125 and AdoMet effects on the apoptotic signaling pathway were determined by Western blot analysis of cytochrome c release and pro-caspase 3 fragmentation. The AdoMet effect on glutathione levels was measured by Ellman's method and reactive oxygen species (ROS) generation by cell cytometry.RESULTS: The exposure of hepatocytes to ethanol induced JNK activation, c-jun phosphorylation, Bid fragmentation, cytochrome c release and pro-caspase 3 cleavage; these effects were diminished by SP600125, and caused a significant decreasein ethanol-induced apoptosis (P< 0.05). AdoMet exerted an antioxidant effect maintaining glutathione levels and decreasing ROS generation, without a significant effect on JNK activity,and prevented cytochrome c release and pro-caspase 3 cleavage.CONCLUSION: The JNK signaling cascade is a key component of the proapoptotic signaling pathway induced by ethanol. JNK activation may be independent from ROS generation, since AdoMet which exerted antioxidant properties did not have a significant effect on JNK activity. JNK pathway modulator agents and AdoMet may be components of promising therapies for alcoholic liver disease (ALD) treatment.

  12. Protective role of ellagitannins from Eucalyptus citriodora against ethanol-induced gastric ulcer in rats: impact on oxidative stress, inflammation and calcitonin-gene related peptide.

    Al-Sayed, Eman; El-Naga, Reem N

    2015-01-15

    The gastroprotective activity of an ellagitannin-rich fraction obtained from Eucalyptus citriodora (ECF) was investigated against ethanol-induced gastric ulceration in rats. The rats were pretreated with ECF (25, 50 and 100mg/kg) 1h before the administration of absolute ethanol to induce acute gastric ulceration. The gastric lesions were significantly reduced by all doses of ECF. Notably, pre-treatment with ECF (100mg/kg) conferred 99.6% gastroprotection, which is significantly higher than that produced by omeprazole. Moreover, ECF administration markedly increased the mucin content in a dose-dependent manner. The potent gastroprotective effect of ECF could be partly mediated by attenuating ethanol-induced oxidative stress. ECF-pre-treatment markedly increased the depleted GSH and SOD levels in a dose-dependent manner. Moreover, ECF significantly decreased the elevated MDA tissue levels induced by ethanol administration. The results demonstrated that ECF administration exerted a powerful anti-inflammatory activity as evidenced by the reduction in the pro-inflammatory markers; IL-1β, TNF-α, 5-LO and COX-2. Additionally, the caspase-3 tissue levels were significantly reduced in the groups pre-treated with ECF. These results suggest that ECF could exert a beneficial gastroprotective effect through their antioxidant, anti-inflammatory and anti-apoptotic properties. Furthermore, ECF pre-treatment significantly attenuated the ethanol-induced decrease in CGRP expression, which has a protective role against gastric ulceration. Histopathological examination revealed intact mucosal layer, absence of hemorrhage and necrosis in groups treated with ECF. Ellagitannins were identified as the major active constituents responsible for the marked antioxidant and gastroprotective properties of ECF. The HPLC-PDA-ESI/MS/MS technique was employed to identify the ellagitannins of E. citriodora. PMID:25636864

  13. Acute myocardial infarct imaging

    A brief review is presented of radiopharmaceuticals used for imaging acute myocardial infarction and instrumentation using the rectilinear scanner and the scintillation camera. Clinical experience indicates that myocardial imaging with /sup 99 m/Tc pyrophosphate is a useful adjunct to the electrocardiogram and serum enzyme activity in managing patients with myocardial infarction. The technique allows rapid diagnosis, accurate localization, and an estimate of the size of acute infarcts. It can also be used to document infarct extension and in association with myocardial perfusion imaging can help differentiate fresh from old myocardial infarction

  14. Ethanol Induced Toxicity and Lipid Peroxidation in Pregnant Mice: Protective Effects of Butanolic Extract from Leaves of Chrysanthemum fontanesii, Vitamin E and C

    Amel Amrani; Nassima Boubekri; Ouahiba Benaissa; Djamila Zama; Fadila Benayache; Samir Benayache

    2014-01-01

    Background: The objective of the present study was to investigate the ability of butanolic extract from leaves of Chrysanthemum fontanesii, vitamin E and C to modulate ethanol-Induced toxicity and oxidation damage in maternal and fetal tissues of mice. Butanolic extract from leaves of Chrysanthemum fontanesii (200 mg/Kg per day), vitamin E (100mg/Kg per day) and C (8.3mg/Kg per day) were administered by gavage to groups of pregnant mice from the 6 th to 17 th day of gestation. A number of ani...

  15. Ethanol activation of protein kinase A regulates GABA-A receptor subunit expression in the cerebral cortex and contributes to ethanol-induced hypnosis

    A LeslieMorrow

    2012-04-01

    Full Text Available Protein kinases are implicated in neuronal cell functions such as modulation of ion channel function, trafficking and synaptic excitability. Both protein kinase C (PKC and A (PKA are involved in regulation of γ-aminobutyric acid type A (GABA-A receptors through phosphorylation. However, the role of PKA in regulating GABA-A receptors following acute ethanol exposure is not known. The present study investigated the role of PKA in ethanol effects on GABA-A receptor α1 subunit expression in the P2 synaptosomal fraction of the rat cerebral cortex. Additionally, GABA-related behaviors were also examined. Rats were administered ethanol (2.0 – 3.5 g/kg or saline and PKC, PKA and GABA-A receptor α1 subunit levels were measured by Western blot analysis. Ethanol (3.5 g/kg transiently increased GABA-A receptor α1 subunit expression and PKA RIIβ subunit expression at similar time points whereas PKA RIIα was increased at later time points. In contrast, PKC isoform expression remained unchanged. Notably, the moderate ethanol dose (2.0g/kg had no effect on GABA-A α1 subunit levels although PKA RIIα and RIIβ were increased at 10 and 60 minutes, when PKC isozymes are also known to be elevated. To determine if PKA activation was responsible for the ethanol-induced elevation of GABA-A α1 subunits, the PKA antagonist H89 was administered to rats prior to ethanol exposure. H89 administration prevented ethanol-induced increases in GABA-A receptor α1 subunit expression. Moreover, increasing PKA activity intracerebroventricularly with Sp-cAMP prior to a hypnotic dose of ethanol increased ethanol-induced loss of righting reflex duration. This effect appears to be mediated in part by GABA-A receptors as increasing PKA activity also increased the duration of muscimol-induced loss of righting reflex. Overall these data suggest that PKA mediates ethanol-induced GABA-A receptor expression and contributes to ethanol behavioral effects involving GABA-A receptors.

  16. Binge ethanol exposure increases the Krüppel-like factor 11-monoamine oxidase (MAO) pathway in rats: Examining the use of MAO inhibitors to prevent ethanol-induced brain injury.

    Duncan, Jeremy W; Zhang, Xiao; Wang, Niping; Johnson, Shakevia; Harris, Sharonda; Udemgba, Chinelo; Ou, Xiao-Ming; Youdim, Moussa B; Stockmeier, Craig A; Wang, Jun Ming

    2016-06-01

    Binge drinking induces several neurotoxic consequences including oxidative stress and neurodegeneration. Because of these effects, drugs which prevent ethanol-induced damage to the brain may be clinically beneficial. In this study, we investigated the ethanol-mediated KLF11-MAO cell death cascade in the frontal cortex of Sprague-Dawley rats exposed to a modified Majchowicz 4-day binge ethanol model and control rats. Moreover, MAO inhibitors (MAOIs) were investigated for neuroprotective activity against binge ethanol. Binge ethanol-treated rats demonstrated a significant increase in KLF11, both MAO isoforms, protein oxidation and caspase-3, as well as a reduction in BDNF expression in the frontal cortex compared to control rats. MAOIs prevented these binge ethanol-induced changes, suggesting a neuroprotective benefit. Neither binge ethanol nor MAOI treatment significantly affected protein expression levels of the oxidative stress enzymes, SOD2 or catalase. Furthermore, ethanol-induced antinociception was enhanced following exposure to the 4-day ethanol binge. These results demonstrate that the KLF11-MAO pathway is activated by binge ethanol exposure and MAOIs are neuroprotective by preventing the binge ethanol-induced changes associated with this cell death cascade. This study supports KLF11-MAO as a mechanism of ethanol-induced neurotoxicity and cell death that could be targeted with MAOI drug therapy to alleviate alcohol-related brain injury. Further examination of MAOIs to reduce alcohol use disorder-related brain injury could provide pivotal insight to future pharmacotherapeutic opportunities. PMID:26805422

  17. True-3D accentuating of grids and streets in urban topographic maps enhances human object location memory.

    Dennis Edler

    Full Text Available Cognitive representations of learned map information are subject to systematic distortion errors. Map elements that divide a map surface into regions, such as content-related linear symbols (e.g. streets, rivers, railway systems or additional artificial layers (coordinate grids, provide an orientation pattern that can help users to reduce distortions in their mental representations. In recent years, the television industry has started to establish True-3D (autostereoscopic displays as mass media. These modern displays make it possible to watch dynamic and static images including depth illusions without additional devices, such as 3D glasses. In these images, visual details can be distributed over different positions along the depth axis. Some empirical studies of vision research provided first evidence that 3D stereoscopic content attracts higher attention and is processed faster. So far, the impact of True-3D accentuating has not yet been explored concerning spatial memory tasks and cartography. This paper reports the results of two empirical studies that focus on investigations whether True-3D accentuating of artificial, regular overlaying line features (i.e. grids and content-related, irregular line features (i.e. highways and main streets in official urban topographic maps (scale 1/10,000 further improves human object location memory performance. The memory performance is measured as both the percentage of correctly recalled object locations (hit rate and the mean distances of correctly recalled objects (spatial accuracy. It is shown that the True-3D accentuating of grids (depth offset: 5 cm significantly enhances the spatial accuracy of recalled map object locations, whereas the True-3D emphasis of streets significantly improves the hit rate of recalled map object locations. These results show the potential of True-3D displays for an improvement of the cognitive representation of learned cartographic information.

  18. True-3D accentuating of grids and streets in urban topographic maps enhances human object location memory.

    Edler, Dennis; Bestgen, Anne-Kathrin; Kuchinke, Lars; Dickmann, Frank

    2015-01-01

    Cognitive representations of learned map information are subject to systematic distortion errors. Map elements that divide a map surface into regions, such as content-related linear symbols (e.g. streets, rivers, railway systems) or additional artificial layers (coordinate grids), provide an orientation pattern that can help users to reduce distortions in their mental representations. In recent years, the television industry has started to establish True-3D (autostereoscopic) displays as mass media. These modern displays make it possible to watch dynamic and static images including depth illusions without additional devices, such as 3D glasses. In these images, visual details can be distributed over different positions along the depth axis. Some empirical studies of vision research provided first evidence that 3D stereoscopic content attracts higher attention and is processed faster. So far, the impact of True-3D accentuating has not yet been explored concerning spatial memory tasks and cartography. This paper reports the results of two empirical studies that focus on investigations whether True-3D accentuating of artificial, regular overlaying line features (i.e. grids) and content-related, irregular line features (i.e. highways and main streets) in official urban topographic maps (scale 1/10,000) further improves human object location memory performance. The memory performance is measured as both the percentage of correctly recalled object locations (hit rate) and the mean distances of correctly recalled objects (spatial accuracy). It is shown that the True-3D accentuating of grids (depth offset: 5 cm) significantly enhances the spatial accuracy of recalled map object locations, whereas the True-3D emphasis of streets significantly improves the hit rate of recalled map object locations. These results show the potential of True-3D displays for an improvement of the cognitive representation of learned cartographic information. PMID:25679208

  19. Gastroprotective Effects of Lion's Mane Mushroom Hericium erinaceus (Bull.:Fr.) Pers. (Aphyllophoromycetideae) Extract against Ethanol-Induced Ulcer in Rats.

    Wong, Jing-Yang; Abdulla, Mahmood Ameen; Raman, Jegadeesh; Phan, Chia-Wei; Kuppusamy, Umah Rani; Golbabapour, Shahram; Sabaratnam, Vikineswary

    2013-01-01

    Hericium erinaceus is a famous tonic in oriental medicine. The gastroprotective effects of aqueous extract of H. erinaceus against ethanol-induced ulcers in Sprague Dawley rats were investigated. The possible involvements of lipid peroxidation, superoxide dismutase, and catalase were also investigated. Acute toxicity study was performed. The effects of aqueous extract of H. erinaceus on the ulcer areas, ulcer inhibition, gastric wall mucus, gross and histological gastric lesions, antioxidant levels, and malondialdehyde (MDA) contents were evaluated in ethanol-induced ulcer in vivo. In acute toxicity study, a high dose of 5 g/kg did not manifest any toxicological signs in rats. The extract promoted ulcer protection as ascertained by a significant reduction of the ulcer area. Furthermore, it exhibited a significant protection activity against gastric mucosal injury by preventing the depletion of antioxidant enzymes. The level of MDA was also limited in rat stomach tissues when compared with the ulcer control group. Immunohistochemistry showed upregulation of HSP70 protein and downregulation of BAX protein in rats pretreated with the extract. The aqueous extract of H. erinaceus protected gastric mucosa in our in vivo model. It is speculated that the bioactive compounds present in the extract may play a major role in gastroprotective activity. PMID:24302966

  20. Anti-Ulcerogenic Properties of Lycium chinense Mill Extracts against Ethanol-Induced Acute Gastric Lesion in Animal Models and Its Active Constituents.

    Olatunji, Opeyemi J; Chen, Hongxia; Zhou, Yifeng

    2015-01-01

    The objective of this study was to explore the gastroprotective properties of the aerial part of Lycium chinense Mill (LCA) against ethanol-induced gastric mucosa lesions in mice models. Administration of LCA at doses of 50, 100, 200 and 400 mg/kg body weight prior to ethanol consumption dose dependently inhibited gastric ulcers. The gastric mucosal injury was analyzed by gastric juice acidity, glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO) activities. Furthermore, the levels of the inflammatory mediators, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in serum were also analyzed using ELISA. Pathological changes were also observed with the aid of hematoxylin-eosin (HE) staining. Our results indicated that LCA significantly reduced the levels of MPO, MDA and increased SOD and GSH activities. Furthermore, LCA also significantly inhibited the levels of TNF-α, IL-6, and IL-1β in the serum of ulcerated mice in a dose dependent manner. Immunohistological analysis indicated that LCA also significantly attenuated the overexpression of nuclear factor-κB in pretreated mice models. This findings suggests Lycium chinense Mill possesses gastroprotective properties against ethanol-induced gastric injury and could be a possible therapeutic intervention in the treatment and management of gastric ulcers. PMID:26694339

  1. Sex differences in the effects of ethanol pre-exposure during adolescence on ethanol-induced conditioned taste aversion in adult rats.

    Sherrill, Luke K; Berthold, Claire; Koss, Wendy A; Juraska, Janice M; Gulley, Joshua M

    2011-11-20

    Alcohol use, which typically begins during adolescence and differs between males and females, is influenced by both the rewarding and aversive properties of the drug. One way adolescent alcohol use may modulate later consumption is by reducing alcohol's aversive properties. Here, we used a conditioned taste aversion (CTA) paradigm to determine if pre-exposure to alcohol (ethanol) during adolescence would attenuate ethanol-induced CTA assessed in adulthood in a sex-dependent manner. Male and female Long-Evans rats were given intraperitoneal (i.p.) injections of saline or 3.0g/kg ethanol in a binge-like pattern during postnatal days (PD) 35-45. In adulthood (>PD 100), rats were given access to 0.1% saccharin, followed by saline or ethanol (1.0 or 1.5g/kg, i.p.), over four conditioning sessions. We found sex differences in ethanol-induced CTA, with males developing a more robust aversion earlier in conditioning. Sex differences in the effects of pre-exposure were also evident: males, but not females, showed an attenuated CTA in adulthood following ethanol pre-exposure, which occurred approximately nine weeks earlier. Taken together, these findings indicate that males are more sensitive to the aversive properties of ethanol than females. In addition, the ability of pre-exposure to the ethanol US to attenuate CTA is enhanced in males compared to females. PMID:21767576

  2. Anti-Ulcerogenic Properties of Lycium chinense Mill Extracts against Ethanol-Induced Acute Gastric Lesion in Animal Models and Its Active Constituents

    Opeyemi J. Olatunji

    2015-12-01

    Full Text Available The objective of this study was to explore the gastroprotective properties of the aerial part of Lycium chinense Mill (LCA against ethanol-induced gastric mucosa lesions in mice models. Administration of LCA at doses of 50, 100, 200 and 400 mg/kg body weight prior to ethanol consumption dose dependently inhibited gastric ulcers. The gastric mucosal injury was analyzed by gastric juice acidity, glutathione (GSH, superoxide dismutase (SOD, malondialdehyde (MDA, myeloperoxidase (MPO activities. Furthermore, the levels of the inflammatory mediators, tumor necrosis factor-α (TNF-α, interleukin-6 (IL-6 and interleukin-1β (IL-1β in serum were also analyzed using ELISA. Pathological changes were also observed with the aid of hematoxylin-eosin (HE staining. Our results indicated that LCA significantly reduced the levels of MPO, MDA and increased SOD and GSH activities. Furthermore, LCA also significantly inhibited the levels of TNF-α, IL-6, and IL-1β in the serum of ulcerated mice in a dose dependent manner. Immunohistological analysis indicated that LCA also significantly attenuated the overexpression of nuclear factor-κB in pretreated mice models. This findings suggests Lycium chinense Mill possesses gastroprotective properties against ethanol-induced gastric injury and could be a possible therapeutic intervention in the treatment and management of gastric ulcers.

  3. Unlocking the Sporicidal Potential of Ethanol: Induced Sporicidal Activity of Ethanol against Clostridium difficile and Bacillus Spores under Altered Physical and Chemical Conditions.

    Michelle M Nerandzic

    Full Text Available Due to their efficacy and convenience, alcohol-based hand sanitizers have been widely adopted as the primary method of hand hygiene in healthcare settings. However, alcohols lack activity against bacterial spores produced by pathogens such as Clostridium difficile and Bacillus anthracis. We hypothesized that sporicidal activity could be induced in alcohols through alteration of physical or chemical conditions that have been shown to degrade or allow penetration of spore coats.Acidification, alkalinization, and heating of ethanol induced rapid sporicidal activity against C. difficile, and to a lesser extent Bacillus thuringiensis and Bacillus subtilis. The sporicidal activity of acidified ethanol was enhanced by increasing ionic strength and mild elevations in temperature. On skin, sporicidal ethanol formulations were as effective as soap and water hand washing in reducing levels of C. difficile spores.These findings demonstrate that novel ethanol-based sporicidal hand hygiene formulations can be developed through alteration of physical and chemical conditions.

  4. Ethanol Induced Toxicity and Lipid Peroxidation in Pregnant Mice: Protective Effects of Butanolic Extract from Leaves of Chrysanthemum fontanesii, Vitamin E and C

    Amel Amrani

    2014-05-01

    Full Text Available Background: The objective of the present study was to investigate the ability of butanolic extract from leaves of Chrysanthemum fontanesii, vitamin E and C to modulate ethanol-Induced toxicity and oxidation damage in maternal and fetal tissues of mice. Butanolic extract from leaves of Chrysanthemum fontanesii (200 mg/Kg per day, vitamin E (100mg/Kg per day and C (8.3mg/Kg per day were administered by gavage to groups of pregnant mice from the 6 th to 17 th day of gestation. A number of animals received plant extract, vitamin E and C, also treated with an oral administration of ethanol (0.02ml/g of 25% v/v absolute ethanol in water per day in same conditions. On day 18 of gestation, pregnant mice were killed, fetus, placenta, fetal liver, liver, kidneys and brain were removed, homogenised and used for determination of lipid peroxidation (LPO using TBARS method. Embryotoxicity was assessed by counting the number of live and dead fetus and growth retardation. Results: Severe alterations in all biomarkers were observed after injury with ETOH. ETOH produced significant decreases in fetal weight and significant increases in embryolethality and lipid peroxidation relative to control values. Treatment with Chrysanthemum fontanesii extract, vitamin C and vitamin E resulted in markedly decreased embryolethality and fetal growth retardation, while increased fetal weight were observed. Conclusion: The butanolic extract from leaves of Chrysanthemum fontanesii, vitamin E and C protected against ethanol induce fetal and maternal toxicity as revealed by the decrease in the extent of lipid peroxidation. So that butanolic extract from leaves of Chrysanthemum fontanesii posses in vivo antioxidant properties.

  5. Acute myocardial infarction:myocardial salvage assessment

    NSENGIYUMVA Pierre; CHEN Li-juan; MA Gen-shan

    2015-01-01

    Primary coronary revascularization by means of percutaneous coronary intervention ( PCI) is a highly ef-fective treatment of acute myocardial infarction re-establishing coronary perfusion and stopping the ongoing necrosis in the dependent myocardium .Single-photon emission computed tomography ( SPECT) is the most widely used mo-dality assessing myocardial salvage as the difference between the acute perfusion defect before intervention and the remaining scar size measured in a second scan several days after the event .SPECT allows quantification of area at risk( AAR) and final infarct size ( FIS) by tracer injection prior to revascularization and after 1 month, respective-ly.SPECT provides the most validated measure of myocardial salvage and has been utilized in multiple randomized clinical trials.However, SPECT is logistically challenging , expensive, and includes radiation exposure .More re-cently, a large number of studies have suggested that cardiac magnetic resonance ( CMR) can determine salvage in a single examination by combining measures of myocardial oedema in the AAR exposed to ischaemia reperfusion with FIS quantification by late gadolinium enhancement .

  6. C/EBP beta and C/EBP delta expression is elevated in the early phase of ethanol-induced hepatosteatosis in mice

    Yu-hsuan CHEN; Chih-min YANG; Shih-pei CHANG; Miao-lin HU

    2009-01-01

    Aim: Alcohol, which is predominantly metabolized in the liver, is a major hepatic toxicant that readily induces hepatic steatosis.The expression of CCAAT enhancer binding protein (C/EBP), especially the C/EBP delta variety, is increased in the early phase of adipogenesis. However, the role of C/EBP delta in ethanol-induced hepatosteatosis is unclear.Methods: Male C57BL/6J mice were randomized to one of four groups: a control group, a group receiving orally administered ethanol (4 g ethanol/kg body weight) (EtOH), a high-fat-diet (HF) group and an EtOH+HF group. Mice were sacrificed after 5 or 10 weeks for various measurements. The in vitro effect of ethanol on the expression of C/EBP alpha, beta and delta was studied in HepG2 cells. Results: By week 5, ethanol treatment had significantly increased liver C/EBP delta and beta protein expression (by 2.3- and 1.4-fold,respectively), which then returned to the control level by week 10. In contrast, the expression of C/EBP alpha was evident only at week 10. The in vitro study shows that C/EBP delta expression was elevated significantly at 24 h but not at 48 or 72 h. C/EBP beta expres-sion was highest at 48 h, whereas C/EBP alpha expression was highest at 72 h. We also found that a low concentration of ethanol plus oleic acid enhanced C/EBP delta expression in HepG2 cells.Conclusion: C/EBP delta expression appears to play an important role in the early phase of ethanol-induced hepatosteatosis in mice and in ethanol-treated HepG2 cells. In addition, EtOH+HF enhances the expression of C/EBP delta in HepG2 cells. Thus, C/EBP delta might be a therapeutic target in alcoholic hepatosteatosis.

  7. Betulin and betulinic acid attenuate ethanol-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS), cytokine (TNF-α, TGF-β) production and by influencing intracellular signaling

    Background/aims: Liver fibrosis has been reported to be inhibited in vivo by oleanolic and ursolic acids. However, the mechanisms of the action of those triterpenoids are poorly understood. In this study, we aimed to determine the antifibrotic potential of other triterpenes, betulin and betulinic acid, and to characterize their influence on the signal transduction pathways involved in ethanol-activated hepatic stellate cells (HSCs). Methods: Investigated was the influence of preincubation of rat HSCs with betulin and betulinic acid, at non-toxic concentrations, on ethanol-induced toxicity, migration, and several markers of HSC activation such as smooth muscle α-actin (α-SMA) and procollagen I expression, release of reactive oxygen species (ROS) and cytokines: tumor necrosis factor-α (TNF-α) and tumor growth factor-β1 (TGF-β1), and production of metalloproteinase-2 (MMP-2) and tissue inhibitors of metalloproteinases (TIMP-1 and TIMP-2). To assess the mechanism of the action of those triterpenes, intracellular signals such as nuclear factor-κB (NFκB), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) induced by ethanol were examined. Results: In vitro, betulin, but not betulinic acid, protected HSCs against ethanol toxicity. However, both betulin and betulinic acid inhibited the production of ROS by HSCs treated with ethanol and inhibited their migration as well as ethanol-induced TNF-α, and TGF-β1, production. Betulin and betulinic acid down-regulated ethanol-induced production of TIMP-1 and TIMP-2. Betulin and betulinic acid, also decreased ethanol-induced activity of MMP-2. In ethanol-induced HSCs, betulin inhibited the activation of the p38 MAPK and the JNK transduction pathways, while betulinic acid inhibited the JNK transduction pathway only. They also significantly inhibited phosphorylation of IκB and Smad 3 and attenuated the activation of TGF-β1 and NFκB/IκB transduction signaling. Conclusion: The results

  8. Gastroprotection of Suaveolol, Isolated from Hyptis suaveolens, against Ethanol-Induced Gastric Lesions in Wistar Rats: Role of Prostaglandins, Nitric Oxide and Sulfhydryls

    María Elena Sánchez-Mendoza

    2012-07-01

    Full Text Available Hyptis suaveolens is a medicinal plant that is, according to traditional medicine, considered useful in the treatment of gastric ulcers. Although its gastroprotective activity was reported, the active compounds have not been identified. Therefore, the aim of the present study was to identify at least one active compound potentially responsible for the gastroprotective activity of H. suaveolens by using a bioassay guided study with an ethanol-induced gastric ulcer experimental model in rats. The results show that the hexane extract had protective activity (close to 70% when using doses between 10 and 100 mg/kg, and that the compound suaveolol, isolated from this extract, was one of the active gastroprotective agents. This is the first report about the gastroprotective activity of suaveolol. Rats treated with this compound at 3, 10, 30 and 100 mg/kg showed 12.6, 21.3, 39.6 and 70.2% gastroprotection respectively. The effect elicited by suaveolol (at 100 mg/kg was attenuated by pretreatment with either NG-nitro-L-arginine methyl ester (70 mg/kg, i.p., a nitric oxide (NO synthase inhibitor, indomethacin (10 mg/kg, s.c., a blocker of prostaglandin synthesis, or N-ethylmaleimide (10 mg/kg, s.c., a blocker of sulfhydryl groups. This suggests that the gastroprotective mechanism of action of this compound involves NO, prostaglandins and sulfhydryl groups.

  9. Gastroprotective and Anti-ulcer activity of Aloe vera juice, Papaya fruit juice and Aloe vera and Papaya fruit combined juice in Ethanol induced Ulcerated Rats

    S. Gopinathan

    2013-12-01

    Full Text Available Peptic ulcer is the most prevalent gastrointestinal disease. Even though a wide range of drugs are available for the treatment of peptic ulcer, but many of these do not fulfill all the requirements and have side effects. These factors have attracted researchers to investigate the natural products which have more efficacy, less side effects and less expensive for the treatment of peptic ulcer disease. In the present study the anti ulcer activity of (1 Aloe vera juice, (2 papaya fruit juice (3 Aloe vera and papaya fruit combined juice were investigated in the ethanol induced ulcerated rats. The administration of plant juices decreased the offensive factors like ulcer index and acid secretion and also reduced the amount of protein and carbohydrates in the stomach fluid. Further, plant juices increased the defensive factors like activity of oxidative enzymes such as superoxide dismutase and reduced glutathione. Activities of alkaline phosphatase and lipid peroxide were higher in the diseased condition and same were reduced after the treatment with plant juices. Content of haemoglobin and RBC and WBC counts were brought back to normalcy after the treatment with plant juices. The efficacy of plant juices was comparable with the reference drug- Ranitidine. The results of the present study reveal that the plant juices are having efficiency in the gastroprotective activity. It is recommended that the above said plant juices can be further studied for their anti ulcer efficacy in human subjects.

  10. Heroin Abuse and Myocardial Infarction

    Tatli, Ersan; Aktoz, Meryem

    2010-01-01

    Information concerning acute myocardial infarction after heroin usage is limited and the actual mechanism of heroin-induced myocardial infarction is not well known. Only one report has been described noting the association between usage heroin and acute myocardial infarction in a young man with normal coronary arteries. We also reported a patient with normal coronary arteries and acute myocardial infarction after heroin abuse. Eroin kullanımı sonrası akut miyokard inf...

  11. Evaluation of Cytoprotection Against Ethanol-induced Injury in Gastric Mocosa Pretreated with Honey Alone, Honey in Combination with Ocimum bacilicum Oil or Honey in Combination with Cimetidine in Rats

    K.A.R.Suzainur

    2005-01-01

    Full Text Available Honey alone or, honey in combination with O. bacilicum oil or with cimitidine was found to posse`s significant anti-ulcer activity against ethanol-induced ulceration in experimental animal models macroscopically and microscopically. Significant inhibition was observed against ethanol-induced ulceration. Macroscopically, oral administration of absolute ethanol (5 ml kg-1 body weight to fasted rats produced extensive hemorrhagic lesions of gastric mucosa. Pretreatment with honey alone (5 ml kg-1 body weight or honey in combination with O. bacilicum oil extracts (5 ml kg-1 body weight or honey in combination with cimitidine (5 ml kg-1 body weight orally 30 minutes before administration of absolute alcohol significantly prevent or reduced the formation of such lesion. Microscopically, pretreatment rats showed significantly marked inhibition or reduction of gastric damage and no submucosal edema or leucocytes infiltration.

  12. Lesions of the Lateral Habenula Increase Voluntary Ethanol Consumption and Operant Self-Administration, Block Yohimbine-Induced Reinstatement of Ethanol Seeking, and Attenuate Ethanol-Induced Conditioned Taste Aversion

    Haack, Andrew K.; Sheth, Chandni; Schwager, Andrea L.; Sinclair, Michael S.; Tandon, Shashank; Taha, Sharif A.; ,

    2014-01-01

    The lateral habenula (LHb) plays an important role in learning driven by negative outcomes. Many drugs of abuse, including ethanol, have dose-dependent aversive effects that act to limit intake of the drug. However, the role of the LHb in regulating ethanol intake is unknown. In the present study, we compared voluntary ethanol consumption and self-administration, yohimbine-induced reinstatement of ethanol seeking, and ethanol-induced conditioned taste aversion in rats with sham or LHb lesions...

  13. Does impaired O2 delivery during exercise accentuate central and peripheral fatigue in patients with coexistent COPD-CHF?

    Oliveira, Mayron F; Zelt, Joel T J; Jones, Joshua H; Hirai, Daniel M; O'Donnell, Denis E; Verges, Samuel; Neder, J Alberto

    2014-01-01

    Impairment in oxygen (O2) delivery to the central nervous system ("brain") and skeletal locomotor muscle during exercise has been associated with central and peripheral neuromuscular fatigue in healthy humans. From a clinical perspective, impaired tissue O2 transport is a key pathophysiological mechanism shared by cardiopulmonary diseases, such as chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF). In addition to arterial hypoxemic conditions in COPD, there is growing evidence that cerebral and muscle blood flow and oxygenation can be reduced during exercise in both isolated COPD and CHF. Compromised cardiac output due to impaired cardiopulmonary function/interactions and blood flow redistribution to the overloaded respiratory muscles (i.e., ↑work of breathing) may underpin these abnormalities. Unfortunately, COPD and CHF coexist in almost a third of elderly patients making these mechanisms potentially more relevant to exercise intolerance. In this context, it remains unknown whether decreased O2 delivery accentuates neuromuscular manifestations of central and peripheral fatigue in coexistent COPD-CHF. If this holds true, it is conceivable that delivering a low-density gas mixture (heliox) through non-invasive positive pressure ventilation could ameliorate cardiopulmonary function/interactions and reduce the work of breathing during exercise in these patients. The major consequence would be increased O2 delivery to the brain and active muscles with potential benefits to exercise capacity (i.e., ↓central and peripheral neuromuscular fatigue, respectively). We therefore hypothesize that patients with coexistent COPD-CHF stop exercising prematurely due to impaired central motor drive and muscle contractility as the cardiorespiratory system fails to deliver sufficient O2 to simultaneously attend the metabolic demands of the brain and the active limb muscles. PMID:25610401

  14. Does Impaired O2 Delivery During Exercise Accentuate Central and Peripheral Fatigue in Patients with Coexistent COPD-CHF?

    Mayron F. Oliveira

    2015-01-01

    Full Text Available Impairment in oxygen (O2 delivery to the central nervous system (brain and skeletal locomotor muscle during exercise has been associated with central and peripheral neuromuscular fatigue in healthy humans. From a clinical perspective, impaired tissue O2 transport is a key pathophysiological mechanism shared by cardiopulmonary diseases, such as chronic obstructive pulmonary disease (COPD and chronic heart failure (CHF. In addition to arterial hypoxemic conditions in COPD, there is growing evidence that cerebral and muscle blood flow and oxygenation can be reduced during exercise in both isolated COPD and CHF. Compromised cardiac output due to impaired cardiopulmonary function/interactions and blood flow redistribution to the overloaded respiratory muscles (i.e., ↑work of breathing may underpin these abnormalities. Unfortunately, COPD and CHF coexist in almost a third of elderly patients making these mechanisms potentially more relevant to exercise intolerance. In this context, it remains unknown whether decreased O2 delivery accentuates neuromuscular manifestations of central and peripheral fatigue in coexistent COPD-CHF. If this holds true, it is conceivable that delivering a low-density gas mixture (heliox through non-invasive positive pressure ventilation could ameliorate cardiopulmonary function/interactions and reduce the work of breathing during exercise in these patients. The major consequence would be increased O2 delivery to the brain and active muscles with potential benefits to exercise capacity (i.e., ↓central and peripheral neuromuscular fatigue, respectively. We therefore hypothesize that patients with coexistent COPD-CHF stop exercising prematurely due to impaired central motor drive and muscle contractility as the cardiorespiratory system fails to deliver sufficient O2 to simultaneously attend the metabolic demands of the brain and the active limb muscles.

  15. Measuring myocardial perfusion

    Qayyum, A A; Kastrup, J

    2015-01-01

    . Myocardial perfusion abnormalities are the first sign of the ischaemic cascade in the development of coronary artery disease (CAD). PET is considered the non-invasive clinical reference standard for absolute quantification of myocardial perfusion. The diagnostic and prognostic value of PET is well-known and......-pass of non-ionic and ionic contrast agents, respectively. Absolute quantification with CMR has yet to be established in routine clinical practice, while CT has yet to prove its diagnostic and prognostic value. The upcoming years may change the way we diagnose and treat patients suspected of having CAD...

  16. Instant Stent-Accentuated Three-Dimensional Optical Coherence Tomography Guided Selection of Proper Distal Cell for Side Branch Dilatation in Bifurcation Stenting

    Fumiaki Nakao

    2015-01-01

    In the bifurcation stenting, the distal rewiring for the side branch postdilatation confirmed by two-dimensional modalities may not lead to favorable results in some cases. If there are two distal cells divided by the link bridging from the carina, the rewiring through the larger distal cell may be recommended for the side branch postdilatation. Detailed confirmation of the rewired cell by the intraprocedural instant stent-accentuated three-dimensional optical coherence tomography is important.

  17. Myocardial perfusion SPECT imaging in patients with myocardial bridging

    Objective: Stress myocardial perfusion SPECT imaging was used to assess myocardial ischemia in patients with myocardial bridging. Methods: Ninety-six patients with myocardial bridging of the left anterior descending artery documented by coronary angiography were included in this study. All under- went exercise or pharmacological stress myocardial perfusion SPECT assessing myocardial ischemia. None had prior myocardial infarction. One year follow-up by telephone interview was performed in all patients. Results The mean stenotic severity of systolic phase on angiography was (65 ± 19)%. In the SPECT study, 20 of 96 (20.8%) patients showed abnormal perfusion. This percentage was significantly higher than that of stress electrocardiogram (ECG). The higher positive rate of SPECT perfusion images was showed in the group of patients with severe systolic narrowing (≥75%) than that with mild-to-moderate systolic narrowing (50% vs 6.3%, P<0.001). The prevalence of abnormal image was significantly higher in ELDERLY PEOPLE; patients with STT change on rest ECG than in those with normal rest ECG (54.2% vs 9.7%, P<0.001). During follow-up, one patient with abnormal SPECT perfusion image sustained angina and accepted percutaneous coronary intervention, and no cardiac event occurred in patients with normal images. Conclusions: Stress myocardial perfusion SPECT imaging can be used effectively for assessing myocardial ischemia and has potential prognostic value for patients with myocardial bridging. (authors)

  18. Effect of indole-3-carbinol on ethanol-induced liver injury and acetaldehyde-stimulated hepatic stellate cells activation using precision-cut rat liver slices.

    Guo, Yu; Wu, Xiao-Qian; Zhang, Chun; Liao, Zhang-Xiu; Wu, Yong; Xia, Zheng-Yuan; Wang, Hui

    2010-12-01

    1. Indole-3-carbinol (I3C), a major indole compound found in high levels in cruciferous vegetables, shows a broad spectrum of biological activities. However, few studies have reported the effect of I3C on alcoholic liver injury. In the present study, we investigated the protective effect of I3C on acute ethanol-induced hepatotoxicity and acetaldehyde-stimulated hepatic stellate cells (HSC) activation using precision-cut liver slices (PCLS). 2. Rat PCLS were incubated with 50 mmol/L ethanol or 350 μmol/L acetaldehyde, and different concentrations (100-400 μmol/L) of I3C were added into the culture system of these two liver injury models, respectively. Hepatotoxicity was assessed by measuring enzyme leakage and malondialdehyde (MDA) content in tissue. Activities of alcoholic enzymes were also determined. α-Smooth muscle actin (α-SMA), transforming growth factor (TGF-β(1) ) and hydroxyproline (HYP) were used as indices to evaluate the activation of HSC. In addition, matrix metalloproteinase-1 (MMP-1) and the tissue inhibitor of metalloproteinase (TIMP-1) were observed to estimate collagen degradation. 3. I3C significantly reduced the enzyme leakage in ethanol-treated slices. In I3C groups, cytochrome P450 (CYP) 2E1 activities were inhibited by 40.9-51.8%, whereas alcohol dehydrogenase (ADH) activity was enhanced 1.6-fold compared with the ethanol-treated group. I3C also showed an inhibitory effect against HSC activation and collagen production stimulated by acetaldehyde. After being incubated with I3C (400 μmol/L), the expression of MMP-1 was markedly enhanced, whereas TIMP-1 was decreased. 4. These results showed that I3C protected PCLS against alcoholic liver injury, which might be associated with the regulation of ethanol metabolic enzymes, attenuation of oxidative injury and acceleration of collagen degradation. PMID:20880187

  19. Acute myocardial infarction related to smoke inhalation and myocardial bridging.

    McCabe, M J; Weston, C. F.; Fraser, A G

    1992-01-01

    A previously healthy 26 year old woman who was exposed to smoke during a house fire developed acute anterior myocardial infarction complicated by ventricular fibrillation. Subsequent left ventriculography confirmed anterior infarction, but coronary arteriography was normal apart from myocardial bridging over a segment of the left anterior descending artery. The development of acute myocardial infarction in this patient suggests that, in the presence of bridging, carbon monoxide inhalation may...

  20. Molecular imaging in myocardial fibrosis

    With the development of life science and medical technology, myocardial fibrosis is being increasingly recognized as a new therapeutic target for heart diseases. However, traditional methods for detection of myocardial fibrosis, such as myocardial biopsy and laboratory assay of serum metabolites or enzymes, are not satisfactory in meeting the clinical demands because of their intrinsic limitations. Molecular imaging may non-invasively and quantitatively evaluate the presence/absence, degree and turnover of myocardial fibrosis in vivo with good specificity, thus being useful for clinical assessment and intervention. Currently, the commonly used molecular imaging modalities for evaluation of myocardial fibrosis include SPECT, PET and MRI. It is hopeful that the molecular probe for targeted ultrasound technology may also be developed in the near future. This review highlights the current status and future trends of molecular imaging in myocardial fibrosis. (authors)

  1. Myocardial ischemia in hypertrophic cardiomyopathy

    Myocardial ischemia in hypertrophic cardiomyopathy is multifactorial and explains the occurrence of angina, in about 50% of patients. The pathophysiology of myocardial ischemia may be explained by the increase of the ventricular mass and relative paucity of the coronary microcirculation; the elevated ventricular filling pressures and myocardial stiffness causing a compression of the coronary microvessels; the impaired coronary vasodilator flow reserve caused by anatomic and functional abnormalities; and the systolic compression of epicardial vessel (myocardial bridges). Myocardial ischemia must be investigated by perfusion scintigraphic methods since its presence influences the prognosis and has relevant clinical implications for management of patients. Patients with hypertrophic cardiomyopathy and documented myocardial ischemia usually need to undergo invasive coronary angiography to exclude the presence of concomitant atherosclerotic coronary disease. (author)

  2. Acute myocardial infarction.

    Rischpler, Christoph

    2016-09-01

    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. PMID:27225319

  3. Myocardial energy metabolism

    Myocardial Energy Metabolism offers a scientific survey which may be looked upon as complementary to the classical haemodynamic view of the hart. Sections on Basic mechanisms, Models and techniques, and on Clinical implications make this book a worthwhile acquisition for cardiologists, cardiac surgeons, basic scientists in cardiovascular physiology, as well as for students with a more than average interest in the organ. Not all basic questions with regard to formation, breakdown and usage of energy (ATP) in the hart have been asked or answered, but invited experts from the fields of cardiac biochemistry, (electro)physiology, pharmacology, anaesthesiology and clinical cardiological research have covered the subject extensively from their own points of view. Furthermore, Myocardial Energy Metabolism shows how basic scientific knowledge may be integrated into cardiological practice. The potential that new techniques like NMR and PET-scanning may offer to the cardiologist of the near future becomes particularly clear when the heart is studied with regard to its energy metabolism

  4. SURGERY OF SYMPTOMATIC MYOCARDIAL BRIDGING

    N. Maghamipour N. Safaei

    2007-01-01

    Myocardial bridging with systolic compression of the left anterior descending coronary artery (LAD) may be associated with myocardial ischemia. In symptomatic myocardial bridging unresponsive to medical treatment, surgical unroofing of the left LAD can be performed. Little information is available about the long-term prognosis of patients with this coronary anomaly after the surgical unroofing, so we decided to evaluate the result of this operation. A total of 26 patients underwent surgical u...

  5. Acute Myocardial Infarction 19922001

    Robert Schmitz

    2005-01-01

    Heart disease is the leading cause of hospitalization and death in the United States among persons age 65 and older. Acute myocardial infarction (AMI), more commonly known as heart attack, accounted for more than 321,000 hospitalizations among Medicare beneficiaries in 2001. This report presents trends in AMI hospitalization, readmission, and mortality rates from 1992 through 2001 among Medicare fee-for-service beneficiaries across various demographic groups.

  6. An unusual myocardial infarction

    Di Michele, Sara; MIRABELLI, FRANCESCA; Galzerano, Domenico; Mankad, Sunil

    2014-01-01

    Summary We present a 74-year-old male with a chondrosarcoma, who presented with chest pain. The history, electrocardiogram (ECG), and biomarkers established the diagnosis of myocardial infarction (MI); angiography did not show coronary atherosclerosis and, both initial transthoracic echocardiogram and chest computed tomography (CT), did not demonstrate any cardiac abnormalities. A second echocardiogram following a routine ECG showed presence of a mass involving the right ventricle and the car...

  7. Myocardial protection in sepsis

    Shakar, Simon; Brian D Lowes

    2008-01-01

    Sepsis with myocardial dysfunction is seen commonly. Beta-blockers have been used successfully to treat chronic heart failure based on the premise that chronically elevated adrenergic drive is detrimental to the myocardium. However, recent reports on the acute use of beta-blockers in situations with potential hemodynamic compromise have shown the risks associated with this approach. In critical situations, the main effect of adrenergic activation is to support cardiovascular function. Caution...

  8. Acute myocardial infarction

    De la Vega-Vélez Henrique

    2012-01-01

    The prevalence of the myocardial infarction (MI) was increasing according to the decadesof the 20th century. In the second decade, the electrocardiogram was introduced, animportant diagnostic tool which still has full validity. The professor of the Facultadde Medicina of the Universidad de Cartagena, Colombia, Henrique de la Vega Vélezpublished in 1942 a thematic review that includes three clinical cases of MI. The textallows observing the conceptualization that was managed seventy years ago ...

  9. Myocardial arterial spin labeling

    Kober, Frank; Jao, Terrence; Troalen, Thomas; Nayak, Krishna S.

    2016-01-01

    Arterial spin labeling (ASL) is a cardiovascular magnetic resonance (CMR) technique for mapping regional myocardial blood flow. It does not require any contrast agents, is compatible with stress testing, and can be performed repeatedly or even continuously. ASL-CMR has been performed with great success in small-animals, but sensitivity to date has been poor in large animals and humans and remains an active area of research. This review paper summarizes the development of ASL-CMR techniques, c...

  10. Tert-butylhydroquinone attenuates the ethanol-induced apoptosis of and activates the Nrf2 antioxidant defense pathway in H9c2 cardiomyocytes.

    Shi, Xiaojing; Li, Yang; Hu, Jun; Yu, Bo

    2016-07-01

    Tert-butylhydroquinone (tBHQ), an inducer of nuclear factor erythroid 2-related factor 2 (Nrf2), has been demonstrated to attenuate oxidative stress-induced injury and the apoptosis of human neural stem cells and other cell types. However, whether tBHQ is able to exert a protective effect against oxidative stress and the apoptosis of cardiomyocytes has not yet been determined. Thus, the objective of the present study was to determine whether tBHQ protects H9c2 cardiomyocytes against ethanol-induced apoptosis. For this purpose, four sets of experiments were performed under standard culture conditions as follows: i) untreated control cells; ii) cell treatment with 200 mM ethanol; iii) cell treatment with 5 µM tBHQ; and iv) cell pre-treatment with 5 µM tBHQ for 24 h, followed by medium change and co-culture with 200 mM ethanol containing 5 µM tBHQ for a further 24 h. The viability of the cardiomyocytes was evaluated by 3-(4,5-dimethylthiazol‑2-yl)‑2,5-diphenyltetrazolium bromide (MTT) assay. The levels of intracellular reactive oxygen species (ROS) and apoptosis were assessed by flow cytometry. Protein expression was measured by western blot analysis, and Nrf2 nuclear localization was observed by immunofluorescence. Exposure to ethanol led to a decrease in the protein expression of Nrf2 and its downstream antioxidant enzymes, accompanied by an increase in ROS generation and in the apoptosis of H9c2 cells. Pre-treatment with tBHQ significantly prevented the H9c2 cells from undergoing ethanol‑induced apoptosis. tBHQ also increased the expression of B-cell lymphoma-2 (Bcl-2), whereas Bcl-2-associated X protein (Bax) expression was decreased. tBHQ promoted Nrf2 nuclear localization and increased the expression of Nrf2, superoxide dismutase (SOD), catalase (CAT) and heme oxygenase-1 (HO-1), and simultaneously inhibited the ethanol‑induced overproduction of intracellular ROS. Therefore, tBHQ confers protection against the ethanol

  11. Gastroprotective activity of Annona muricata leaves against ethanol-induced gastric injury in rats via Hsp70/Bax involvement

    Moghadamtousi SZ

    2014-10-01

    Full Text Available Soheil Zorofchian Moghadamtousi,1 Elham Rouhollahi,2 Hamed Karimian,2 Mehran Fadaeinasab,3 Mahmood Ameen Abdulla,2 Habsah Abdul Kadir1 1Biomolecular Research Group, Biochemistry Program, Institute of Biological Sciences, Faculty of Science, 2Department of Biomedical Science, Faculty of Medicine, 3Department of Chemistry, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia Abstract: The popular fruit tree of Annona muricata L. (Annonaceae, known as soursop and graviola, is a widely distributed plant in Central and South America and tropical countries. Leaves of A. muricata have been reported to possess antioxidant and anti-inflammatory activities. In this study, the gastroprotective effects of ethyl acetate extract of A. muricata leaves (EEAM were investigated against ethanol-induced gastric injury models in rats. The acute toxicity test of EEAM in rats, carried out in two doses of 1 g/kg and 2 g/kg, showed the safety of this plant, even at the highest dose of 2 g/kg. The antiulcer study in rats (five groups, n=6 was performed with two doses of EEAM (200 mg/kg and 400 mg/kg and with omeprazole (20 mg/kg, as a standard antiulcer drug. Gross and histological features showed the antiulcerogenic characterizations of EEAM. There was significant suppression on the ulcer lesion index of rats pretreated with EEAM, which was comparable to the omeprazole effect in the omeprazole control group. Oral administration of EEAM to rats caused a significant increase in the level of nitric oxide and antioxidant activities, including catalase, glutathione, and superoxide dismutase associated with attenuation in gastric acidity, and compensatory effect on the loss of gastric wall mucus. In addition, pretreatment of rats with EEAM caused significant reduction in the level of malondialdehyde, as a marker for oxidative stress, associated with an increase in prostaglandin E2 activity. Immunohistochemical staining also demonstrated that EEAM induced the

  12. Protective Effect of Tyrosol and S-Adenosylmethionine against Ethanol-Induced Oxidative Stress of Hepg2 Cells Involves Sirtuin 1, P53 and Erk1/2 Signaling

    Stiuso, Paola; Bagarolo, Maria Libera; Ilisso, Concetta Paola; Vanacore, Daniela; Martino, Elisa; Caraglia, Michele; Porcelli, Marina; Cacciapuoti, Giovanna

    2016-01-01

    Oxidative stress plays a major role in ethanol-induced liver damage, and agents with antioxidant properties are promising as therapeutic opportunities in alcoholic liver disease. In the present work, we investigated the effect of S-adenosylmethionine (AdoMet), Tyrosol (Tyr), and their combination on HepG2 cells exposed to ethanol exploring the potential molecular mechanisms. We exposed HepG2 cells to 1 M ethanol for 4 and 48 h; thereafter, we recorded a decreased cell viability, increase of intracellular reactive oxygen species (ROS) and lipid accumulation, and the release into culture medium of markers of liver disease such as triacylglycerol, cholesterol, transaminases, albumin, ferritin, and homocysteine. On the other hand, AdoMet and Tyrosol were able to attenuate or antagonize these adverse changes induced by acute exposure to ethanol. The protective effects were paralleled by increased Sirtuin 1 protein expression and nuclear translocation and increased ERK1/2 phosphorylation that were both responsible for the protection of cells from apoptosis. Moreover, AdoMet increased p53 and p21 expression, while Tyrosol reduced p21 expression and enhanced the expression of uncleaved caspase 3 and 9, suggesting that its protective effect may be related to the inhibition of the apoptotic machinery. Altogether, our data show that AdoMet and Tyrosol exert beneficial effects in ethanol-induced oxidative stress in HepG2 cells and provide a rationale for their potential use in combination in the prevention of ethanol-induced liver damage. PMID:27128904

  13. Protective Effect of Tyrosol and S-Adenosylmethionine against Ethanol-Induced Oxidative Stress of Hepg2 Cells Involves Sirtuin 1, P53 and Erk1/2 Signaling.

    Stiuso, Paola; Bagarolo, Maria Libera; Ilisso, Concetta Paola; Vanacore, Daniela; Martino, Elisa; Caraglia, Michele; Porcelli, Marina; Cacciapuoti, Giovanna

    2016-01-01

    Oxidative stress plays a major role in ethanol-induced liver damage, and agents with antioxidant properties are promising as therapeutic opportunities in alcoholic liver disease. In the present work, we investigated the effect of S-adenosylmethionine (AdoMet), Tyrosol (Tyr), and their combination on HepG2 cells exposed to ethanol exploring the potential molecular mechanisms. We exposed HepG2 cells to 1 M ethanol for 4 and 48 h; thereafter, we recorded a decreased cell viability, increase of intracellular reactive oxygen species (ROS) and lipid accumulation, and the release into culture medium of markers of liver disease such as triacylglycerol, cholesterol, transaminases, albumin, ferritin, and homocysteine. On the other hand, AdoMet and Tyrosol were able to attenuate or antagonize these adverse changes induced by acute exposure to ethanol. The protective effects were paralleled by increased Sirtuin 1 protein expression and nuclear translocation and increased ERK1/2 phosphorylation that were both responsible for the protection of cells from apoptosis. Moreover, AdoMet increased p53 and p21 expression, while Tyrosol reduced p21 expression and enhanced the expression of uncleaved caspase 3 and 9, suggesting that its protective effect may be related to the inhibition of the apoptotic machinery. Altogether, our data show that AdoMet and Tyrosol exert beneficial effects in ethanol-induced oxidative stress in HepG2 cells and provide a rationale for their potential use in combination in the prevention of ethanol-induced liver damage. PMID:27128904

  14. Novel and quick coronary image analysis by instant stent-accentuated three-dimensional optical coherence tomography system in catheterization laboratory.

    Nakao, Fumiaki; Ueda, Tooru; Nishimura, Shigehiko; Uchinoumi, Hitoshi; Kanemoto, Masashi; Tanaka, Nobuaki; Fujii, Takashi

    2013-07-01

    In order to confirm the relation between stent struts and the jailed side branch (SB), the actual wire re-crossing position and the optimal wire re-crossing position during a bifurcation stenting, we developed the instant stent-accentuated three-dimensional optical coherence tomography (iSA 3D-OCT) system based on a novel algorithm. Stent struts in two-dimensional optical coherence tomography (2D-OCT) are represented as high-intensity line segments or spots in low-intensity background. Stent struts disappear and a vessel image is created by the mean filter followed by the minimum filter. A strut image is created by subtracting a vessel image from an original image, and accentuated. By adding a vessel image to a strut image, iSA 2D-OCT is created. It took only 3 s to accentuate stent struts of 100 frames by ImageJ with its macro program. By the iSA 3D-OCT system which consists of the console of OCT, the USB selector, USB cables, the USB flash drive, the computer, and three freeware programs, it took about 65 s from an export of the image data to an observation of iSA 3D-OCT semi-automatically. During a bifurcation stenting procedure, we could confirm the relation between stent struts and the jailed SB, the actual wire re-crossing position and the optimal wire re-crossing position. Using the iSA 3D-OCT system, a detailed process during a bifurcation PCI can be observed in very short waiting time, about 65 s. It is expected to improve the outcome of a complicated bifurcation PCI by the iSA 3D-OCT system. PMID:23355032

  15. SURGERY OF SYMPTOMATIC MYOCARDIAL BRIDGING

    N. Maghamipour N. Safaei

    2007-06-01

    Full Text Available Myocardial bridging with systolic compression of the left anterior descending coronary artery (LAD may be associated with myocardial ischemia. In symptomatic myocardial bridging unresponsive to medical treatment, surgical unroofing of the left LAD can be performed. Little information is available about the long-term prognosis of patients with this coronary anomaly after the surgical unroofing, so we decided to evaluate the result of this operation. A total of 26 patients underwent surgical unroofing of myocardial bridging. Patients had a myocardial bridge of at least 3 cm in length in the middle of LAD and with more than 70% compression during systole. Unroofing was performed with cardiopulmonary bypass in 16 and with off pump technique in 10 patients. In 6 patients repeat angiographies for control of myotomy were done. In one of them a nonsignificant 20% narrowing was seen. Postoperative scintigraphic and angiographic studies demonstrated restoration of coronary flow and myocardial perfusion without residual myocardial bridges under beta-stimulation in 24 patients. Two patients had residual narrowing. With off pump technique, 1 patient had perforation of the right ventricle and 1 patient underwent reoperation because of incomplete unroofing during the first operation. None of the patients with cardiopulmonary bypass technique had residual chest pain or other complications. Surgical unroofing of myocardial bridging with the aid of cardiopulmonary bypass is a safe and easy procedure with low operative risk and with excellent functional results.

  16. Myocardial perfusion modeling using MRI

    Larsson, H B; Fritz-Hansen, T; Rostrup, Egill;

    1996-01-01

    In the present study, it is shown that it is possible to quantify myocardial perfusion using magnetic resonance imaging in combination with gadolinium diethylenetriaminopentaacetic acid (Gd-DTPA). Previously, a simple model and method for measuring myocardial perfusion using an inversion recovery...

  17. Spiral MR myocardial tagging.

    Ryf, Salome; Kissinger, Kraig V; Spiegel, Marcus A; Börnert, Peter; Manning, Warren J; Boesiger, Peter; Stuber, Matthias

    2004-02-01

    In the present study, complementary spatial modulation of magnetization (CSPAMM) myocardial tagging was extended with an interleaved spiral imaging sequence. The use of a spiral sequence enables the acquisition of grid-tagged images with a tagline distance as low as 4 mm in a single breath-hold. Alternatively, a high temporal resolution of 77 frames per second was obtained with 8-mm grid spacing. Ten healthy adult subjects were studied. With this new approach, high-quality images can be obtained and the tags persist throughout the entire cardiac cycle. PMID:14755646

  18. Assessment of myocardial viability.

    Travin, Mark I; Bergmann, Steven R

    2005-01-01

    The prevalence of left ventricular (LV) dysfunction and resultant congestive heart failure is increasing. Patients with this condition are at high risk for cardiac death and usually have significant limitations in their lifestyles. Although there have been advances in medical therapy resulting in improved survival and well being, the best and most definitive therapy, when appropriate, is revascularization. In the setting of coronary artery disease, accounting for approximately two thirds of cases of congestive heart failure, LV dysfunction often is not the result of irreversible scar but rather caused by impairment in function and energy use of still viable-myocytes, with the opportunity for improved function if coronary blood flow is restored. Patients with LV dysfunction who have viable myocardium are the patients at highest risk because of the potential for ischemia but at the same time benefit most from revascularization. It is important to identify viable myocardium in these patients, and radionuclide myocardial scintigraphy is an excellent tool for this. Single-photon emission computed tomography perfusion scintigraphy, whether using thallium-201, Tc-99m sestamibi, or Tc-99m tetrofosmin, in stress and/or rest protocols, has consistently been shown to be an effective modality for identifying myocardial viability and guiding appropriate management. Metabolic imaging with positron emission tomography radiotracers frequently adds additional information and is a powerful tool for predicting which patients will have an improved outcome from revascularization, including some patients referred instead for cardiac transplantation. Other noninvasive modalities, such as stress echocardiography, also facilitate the assessment of myocardial viability, but there are advantages and disadvantages compared with the nuclear techniques. Nuclear imaging appears to require fewer viable cells for detection, resulting in a higher sensitivity but a lower specificity than stress

  19. MYOCARDIAL INFARCTION TYPE 2. MYTH OR REALITY?

    V. V. Zhelnov; N. V. Dyatlov; L. I. Dvoretsky

    2016-01-01

    According to The Third Definition of Myocardial Infarction there are five types of myocardial infarction depending on pathogenesis. This review provides actual data about myocardial infarction type 2 mechanism including diagnosis management, epidemiological characteristic and patient prognosis. Previously published data shows discordant information about myocardial infarction type 2 frequency, treatment and diagnostic options. Our clinical observation illustrates these severities in diagnosis...

  20. Mechanistic Studies of the Anti-Ulcerogenic Activity and Acute Toxicity Evaluation of Dichlorido-Copper(II-4-(2-5-Bromo-benzylideneaminoethyl Piperazin-1-ium Phenolate Complex against Ethanol-Induced Gastric Injury in Rats

    A. Hamid A. Hadi

    2011-10-01

    Full Text Available The compound dichlorido-copper(II-4-(2-5-bromobenzylideneaminoethyl piperazin-1-ium phenolate (CuLBS was synthesized, characterized and screened for acute toxicity and protective activity against ethanol-induced gastric mucosal injury in rats. Gross microscopic lesions, biochemical and immunological parameters and histochemcial staining of glycogen storage were taken into consideration. Oral administration of CuLBS (30 and 60 mg/Kg for two weeks dose-dependently flattened gastric mucosa, significantly increased gastric mucus and total acidity, compared with control group (P < 0.01. Serum levels of liver enzymes aspartate (AST and alanine transaminases (ALT, pro-inflammatory (IL-6 and TNF-α and anti-inflammatory (IL-10 cytokines in the rats exposed to ethanol induced ulceration have been altered. Administration of CuLBS showed considerable (P < 0.05 protection against ulceration by modulating the acute alterations of cytokines AST, ALT and stomach glycogen. Interestingly, CuLBS did not interfere with the natural release of nitric oxide. CuLBS alone (60 mg/Kg did not exhibit any ulcerogenic effect as assessed using Adami’s scoring scale. An acute toxicity study showed that rats treated with CuLBS (1,000 and 2,000 mg/Kg manifested no abnormal signs. These findings therefore, suggested that the gastroprotective activity of CuLBS might contribute in modulating the inflammatory cytokine-mediated oxidative damage to gastric mucosa.

  1. Valsartan after myocardial infarction.

    Güleç, Sadi

    2014-12-01

    One of the important problems of the patients undergoing acute myocardial infarction (MI) is early development of heart failure. It has been revealed in various studies that renin-angiotensin-aldosterone system (RAAS) has a significant role in this process. The studies conducted with angiotensin converting enzyme (ACE) inhibitors have resulted in decreased mortality rate. Another RAAS blocker which was discovered about ten years later than other ACE inhibitors in historical process is angiotensin receptor blockers (ARB) inhibiting the efficiency of angiotensin 2 by binding to angiotensin 1 receptor. Valsartan is one of the molecules of this group, which has higher number of large-scale randomized clinical studies. In this review, following presentation of a general overview on heart failure after acute MI, the efficiency of ARBs in this patient group will be discussed. This discussion will mostly emphasize the construction, outcomes and clinical importance of VALIANT (VALsartan In Acute myocardial iNfarcTion), which is the study on valsartan after acute MI heart failure. PMID:25604205

  2. Oxytocin ameliorates the immediate myocardial injury in heart transplant through down regulation of the neutrophil dependent myocardial apoptosis

    F Fadhil Al-Amran

    2014-01-01

    Conclusion: Oxytocin ameliorates myocardial injury in heart transplant through down-regulation the myocardial inflammatory response, reactive oxygen species, and neutrophil-dependant myocardial apoptosis.

  3. Myocardial bridging as a cause of acute myocardial infarction: a case report

    Emiroglu Yunus; Gunduz Huseyin; Akdemir Ramazan; Uyan Cihangir

    2002-01-01

    Abstract Background Systolic compression of a coronary artery by overlying myocardial tissue is termed myocardial bridging. Myocardial bridging usually has a benign prognosis, but some cases resulting in myocardial ischemia, infarction and sudden cardiac death have been reported. We are reporting a case of myocardial bridging which was complicated with acute myocardial infarction associated with inappropriate blood donation. Case presentation A 33 year-old-man was admitted to our emergency wi...

  4. Depression following myocardial infarction

    Larsen, Karen Kjær

    2013-01-01

    Myocardial infarction (MI) is a severe life event that is accompanied by an increased risk of depression. Mounting evidence suggests that post-MI depression is associated with adverse outcomes, but the underlying mechanisms of this association remain unclear, and no previous studies have examined...... whether the mental burden of MI is so heavy that it increases the risk of suicide. Although post-MI depression is common and burdensome, the condition remains under-recognised and under-treated. The development of new strategies to improve the quality of care for people with post-MI depression requires...... thorough understanding of the mechanisms that influence the prognosis as well as knowledge of the present care provided. The purpose of this PhD thesis is accordingly subdivided into four specific aims: 1. To estimate the prevalence of depression in people with MI after three months, and to estimate the...

  5. National registry of myocardial infarction

    Amin Daemi; Mehdi Jafari

    2016-01-01

    The Registry of Myocardial Infarctions (MI Registry) is a national registry in Iran that collects and reports the data on myocardial infarctions. Its main advantage is that it covers the whole country and is mandatory for hospitals to register the MI cases in it. Then, the qualified individuals at the provincial and national levels can get intended reports and make appropriate decisions. Such reports, further to the policy makers and managers, can be very valuable for researchers. The regi...

  6. ST elevation without myocardial infarction.

    Bitar, Zouheir Ibrahim; Swede, Mohammad; Almerri, Khaled

    2014-01-01

    Acute myocarditis may mimic myocardial infarction because the affected patients report 'classical' chest pain; the ECG changes and echocardiography are identical to those observed in acute coronary syndromes, and serum markers are increased. We describe a case with ST segment elevation on admission ECG, and coronary angiography was normal. Cardiac magnetic resonance with myocardial delayed enhancement sequences is a non-invasive alternative for diagnosing myocarditis. PMID:24711464

  7. The dipeptidyl peptidase 4 inhibitor vildagliptin does not accentuate glibenclamide-induced hypoglycemia but reduces glucose-induced glucagon-like peptide 1 and gastric inhibitory polypeptide secretion

    El-Ouaghlidi, Andrea; Rehring, Erika; Holst, Jens Juul;

    2007-01-01

    glibenclamide (5 mg), was administered 30 min before 75 g oral glucose. Blood was sampled to measure glucose, and total (sum of active and inactive) GLP-1 and GIP. Statistical evaluation was done using repeated-measures ANOVA. RESULTS: Glibenclamide provoked hypoglycemia (accentuated by the coadministration of vildagliptin. This may be explained by a negative feedback regulation of GLP-1 and GIP secretion that limits the degree to which the active incretin levels are enhanced....

  8. Protective effects of alginate–chitosan microspheres loaded with alkaloids from Coptis chinensis Franch. and Evodia rutaecarpa (Juss. Benth. (Zuojin Pill against ethanol-induced acute gastric mucosal injury in rats

    Wang QS

    2015-11-01

    Full Text Available Qiang-Song Wang,1,2,* Xiao-Ning Zhu,1,* Heng-Li Jiang,1,* Gui-Fang Wang,3 Yuan-Lu Cui1 1Tianjin State Key Laboratory of Modern Chinese Medicine, Research Center of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, 2Institute of Biomedical Engineering, Chinese Academy of Medical Science & Peking Union Medical College, 3Pharmacy Department, Baokang Hospital, Tianjin University of Traditional Chinese Medicine, Tianjin, People’s Republic of China *These authors contributed equally to this work Abstract: Zuojin Pill (ZJP, a traditional Chinese medicine formula, consists of Coptis chinensis Franch. and Evodia rutaecarpa (Juss. Benth. in a ratio of 6:1 (w/w and was first recorded in “Danxi’s experiential therapy” for treating gastrointestinal disorders in the 15th century. However, the poor solubility of alkaloids from ZJP restricted the protective effect in treating gastritis and gastric ulcer. The aim of the study was to investigate the protective mechanism of mucoadhesive microspheres loaded with alkaloids from C. chinensis Franch. and E. rutaecarpa (Juss. Benth. on ethanol-induced acute gastric mucosal injury in rats. Surface morphology, particle size, drug loading, encapsulation efficiency, in vitro drug release, mucoadhesiveness, and fluorescent imaging of the microspheres in gastrointestinal tract were studied. The results showed that the mucoadhesive microspheres loaded with alkaloids could sustain the release of drugs beyond 12 hours and had gastric mucoadhesive property with 82.63% retention rate in vitro. The fluorescence tracer indicated high retention of mucoadhesive microspheres within 12 hours in vivo. The mucoadhesive microspheres loaded with alkaloids could reduce the gastric injury by decreasing the mucosal lesion index, increasing the percentage of inhibition and increasing the amount of mucus in the gastric mucosa in an ethanol-induced gastric mucosal injury rat model. Moreover, the

  9. Myocardial scintigraphy in the diagnosis of myocardial contusion

    To assess the clinical value of a new fatty acid imaging tracer, 123I-β-methyl iodophenyl pentadecanoic acid (BMIPP), I-BMIPP and thallium-201 (Tl) dual imaging was performed at rest in fifteen patients with mild blunt chest trauma (mean AIS thoracic 1.4±0.51, mean ISS 6.47±3.50, mean RTS 7.69±0.43). All patients were prospectively evaluated on the basis of serial electrocardiograms (ECG) and cardiac enzyme studies (total CPK). Tl and BMIPP dual scintigrams were performed within 10 days following admission. SPECT images were divided into seven segments, and the segmental images were visually scored according to tracer uptake on a 3 (severely decreased tracer uptake) to 0 (normal) scale. Nine patients had scintigraphic defects and were considered to have a myocardial contusion. ECG findings, AIS, ISS, and CPK levels failed to distinguish between scintigraphically positive patients and scintigraphically negative patients. Five of the 14 hypoperfused segments on BMIPP imaging, showed normal Tl uptake, one showed lower BMIPP uptake than Tl, and the remaining eight showed similar distribution of both tracers. The mismatch between tracer uptake on BMIPP images and Tl images was thought to reflect impaired myocardial fatty acid metabolism. Thus, mild blunt chest trauma results in a higher frequency of traumatic myocardial injury than previously recognized, and BMIPP is a promising radio-pharmaceutical for evaluating impaired myocardial fatty acid metabolism in patients with myocardial contusion. (author)

  10. Radio-isotopic myocardial study

    The non invasive study of the myocardium with radio-isotopes is effected either with radio-elements labeling on recently infarcted myocardium, such as PYP Tc 99m, or after I.V. injection of Tl 201 extracted by normal myocardium or after I.V. injection of radio-element which study the myocardial metabolism. The fixation of PYP Tc 99m, bordering that of calcium, appears 24 hours after the onset of the myocardial infarction; then it reduces and disappears a week later; its persistency gives evidence of an evolution to ventricular anevrism. The relatively low sensitivity and specificity of this test should induce to reserve if for precise cases. 201 Tl realizes a map of the myocardial flow because this radio-isotope reflects with damping the variations of coronary flow. The scintigraphy is made either after stress test or after I.V. injection of dipyridamole, and the sensitivity and specificity of the test is better than electrocardiographic exercise stress test. The predictive value of the test for a patient highly depends of the prevalence of the coronary disease for this patient; however the results of Tl scintigraphy are far from an ideal test; quantitative or semi-quantitative analysis of the image compared to the analogical image seems to improve sensitivity for detection of coronary disease. After myocardial infarction, its best use is to detect a left anterior descending stenosis after posterior or inferior infarction. Among the possible radio-elements of myocardial metabolism, scintigraphy with fatty acids opens interesting prospects for the study of the myocardial clearance of the radio-isotope, that reflects the global or regional myocardial metabolism

  11. CAD of myocardial perfusion

    Storm, Corstiaan J.; Slump, Cornelis H.

    2007-03-01

    Our purpose is in the automated evaluation of the physiological relevance of lesions in coronary angiograms. We aim to extract as much as possible quantitative information about the physiological condition of the heart from standard angiographic image sequences. Coronary angiography is still the gold standard for evaluating and diagnosing coronary abnormalities as it is able to locate precisely the coronary artery lesions. The dimensions of the stenosis can be assessed nowadays successfully with image processing based Quantitative Coronary Angiography (QCA) techniques. Our purpose is to assess the clinical relevance of the pertinent stenosis. We therefore analyze the myocardial perfusion as revealed in standard angiographic image sequences. In a Region-of-Interest (ROI) on the angiogram (without an overlaying major blood vessel) the contrast is measured as a function of time (the so-called time-density curve). The required hyperemic state of exercise is induced artificially by the injection of a vasodilator drug e.g. papaverine. In order to minimize motion artifacts we select based on the recorded ECG signal end-diastolic images in both a basal and a hyperemic run in the same projection to position the ROI. We present the development of the algorithms together with results of a small study of 20 patients which have been catheterized following the standard protocol.

  12. Myocardial infarction in children: Two interesting cases

    Suryawanshi Suresh

    2011-01-01

    Full Text Available Myocardial infarction in children is extremely rare and can have various etiologies. The following two case reports highlight rare but important causes of myocardial infarction in children.

  13. ANGIOGRAPHIC ASPECTS OF MYOCARDIAL BRIDGES

    Sujatha. M

    2015-12-01

    Full Text Available Introduction: The segment of epicardial coronary artery that traverses intramurally through the myocardium and bridged by a bunch of cardiac muscle fibers is called tunneled artery or intramural artery. The band of cardiac muscle fibers passing over the tunneled artery segment is named as myocardial bridge. During angiography milking effect is observed during systole due to the external pressure of muscle fibers on the tunneled artery that leads to narrowing of vessel lumen and further ischemia. Materials & Methods: It is a prospective study performed from 2012- 2015 in cardiac centers available around Tirupati, Andhra Pradesh, South India. A total number of 2015 adult patients who underwent diagnostic coronary angiography were evaluated to detect myocardial bridges. With the informed consent the relevant data was collected from the patients and analyzed. Results: The prevalence of myocardial bridges was 3.17%. Among the 2015 patients 70.7% are males and 29.2% are females. Among 64 myocardial bridge positive cases 62.5% were male and 37.5% were female patients. Regarding coronary dominance 84% were right dominant and 14.4% were left dominant and 1.6% are balanced. The percentage incidence of myocardial bridging according to dominance was 3.01% for right dominant patients, 4.12% for left dominant patients and 3.1% for balanced dominant patients. In all the myocardial bridge positive cases they were located on the left anterior descending artery (LAD. According to diagnosis the patients with normal coronaries were 22.6%, patients with MILD CAD were 17.9%, patients with single vessel disease were 23.4%, patients with two vessel disease were 14.7% and the patients with triple vessel disease were 21.3%. The 64 myocardial bridging cases were grouped in to three groups according to their age. Incidence of double bridges was observed in 3 cases of which 66.7% males & 33.3% in females. Conclusion: These results show that Andhra Pradesh population are

  14. Acute Myocardial Infarction Due To Electrical Injury

    Uzkeser M et al.

    2011-01-01

    Rhythm abnormalities (conduction defects, tachycardia, and arrhythmia)due to electric shock are common. Rarely, myocardial infarction may beseen in these patients. This situation is generally caused by coronaryartery vasospasm and direct myocardial damage. In this report, wepresent a rare case of myocardial infarction due to electric shock.

  15. Patterns of accentuated grey-white differentiation on diffusion-weighted imaging or the apparent diffusion coefficient maps in comatose survivors after global brain injury

    Aim: To determine what disease entities show accentuated grey-white differentiation of the cerebral hemisphere on diffusion-weighted images (DWI) or apparent diffusion coefficient (ADC) maps, and whether there is a correlation between the different patterns and the cause of the brain injury. Methods and materials: The DWI and ADC maps of 19 patients with global brain injury were reviewed and evaluated to investigate whether there was a correlation between the different patterns seen on the DWI and ADC maps and the cause of global brain injury. The ADC values were measured for quantitative analysis. Results: There were three different patterns of ADC decrease: a predominant ADC decrease in only the cerebral cortex (n = 8; pattern I); an ADC decrease in both the cerebral cortex and white matter (WM) and a predominant decrease in the WM (n = 9; pattern II); and a predominant ADC decrease in only the WM (n = 3; pattern III). Conclusion: Pattern I is cerebral cortical injury, suggesting cortical laminar necrosis in hypoxic brain injury. Pattern II is cerebral cortical and WM injury, frequently seen in brain death, while pattern 3 is mainly WM injury, especially found in hypoglycaemic brain injury. It is likely that pattern I is decorticate injury and pattern II is decerebrate injury in hypoxic ischaemic encephalopathy.Patterns I and II are found in severe hypoxic brain injury, and pattern II is frequently shown in brain death, whereas pattern III was found in severe hypoglycaemic injury.

  16. Mortality rate in type 2 myocardial infarction

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

    2014-01-01

    BACKGROUND: The classification of myocardial infarction into 5 types was introduced in 2007. The prognostic impact of this universal definition, with particular focus on type 2 myocardial infarction, has not been studied prospectively in unselected hospital patients. METHODS: During a 1-year period......, all hospitalized patients having cardiac troponin I measured were considered. The diagnosis of a myocardial infarction was according to the universal definition, and specified criteria were used in the classification of type 2 myocardial infarction. Follow-up was at least 1 year, with mortality as the...... 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....

  17. Dosimetry in myocardial perfusion imaging

    Toledo, Janine M.; Trindade, Bruno; Ribeiro, Tarcisio P.C. [Universidade Federal de Minas Gerais (DEN/UFMG), Belo Horizonte (Brazil). Dept. de Engenharia Nuclear. Programa de Pos-Graduacao em Ciencias e Tecnicas Nucleares

    2011-07-01

    This paper conducts a dosimetric investigation on the myocardial perfusion image protocol, together with a literature reviewing, motivated by the significant statistic increasing on mortality, morbidity and disability associated with cardiovascular disease, surpassing infectious diseases. Nuclear Cardiology plays a role n the diagnostic functional evaluation of the heart and in the prognostic of patients with suspected or known cardiac ischemia. In the context of unstable myocardial ischemic syndrome, myocardial perfusion scintigraphy is a non-invasive procedure performed by administering a radiopharmaceutical targeted to the heart. As tool for this study are that the images obtained by thoracic angiotomography and abdominal aorta as a anatomic and functional information for model reproduction in SISCODES - System of Codes for Absorbed Dose Calculations based on Stochastic Methods. Data were manipulated in order to create a voxel computational model of the heart to be running in MCNP - Monte Carlo Neutron Particle Code. . It was assumed a homogeneous distribution of Tl-201 in cardiac muscle. Simulations of the transport of particles through the voxel and the interaction with the heart tissue were performed. As a result, the isodose curves in the heart model are displayed as well as the dose versus volume histogram of the heart muscle. We conclude that the present computational tools can generate doses distributed in myocardial perfusion. (author)

  18. Dosimetry in myocardial perfusion imaging

    This paper conducts a dosimetric investigation on the myocardial perfusion image protocol, together with a literature reviewing, motivated by the significant statistic increasing on mortality, morbidity and disability associated with cardiovascular disease, surpassing infectious diseases. Nuclear Cardiology plays a role n the diagnostic functional evaluation of the heart and in the prognostic of patients with suspected or known cardiac ischemia. In the context of unstable myocardial ischemic syndrome, myocardial perfusion scintigraphy is a non-invasive procedure performed by administering a radiopharmaceutical targeted to the heart. As tool for this study are that the images obtained by thoracic angiotomography and abdominal aorta as a anatomic and functional information for model reproduction in SISCODES - System of Codes for Absorbed Dose Calculations based on Stochastic Methods. Data were manipulated in order to create a voxel computational model of the heart to be running in MCNP - Monte Carlo Neutron Particle Code. . It was assumed a homogeneous distribution of Tl-201 in cardiac muscle. Simulations of the transport of particles through the voxel and the interaction with the heart tissue were performed. As a result, the isodose curves in the heart model are displayed as well as the dose versus volume histogram of the heart muscle. We conclude that the present computational tools can generate doses distributed in myocardial perfusion. (author)

  19. Accentuation-suppression and scaling

    Sørensen, Thomas Alrik; Bundesen, Claus

    2012-01-01

    The limitations of the visual short-term memory (VSTM) system have become an increasingly popular field of study. One line of inquiry has focused on the way attention selects objects for encoding into VSTM. Using the framework of the Theory of Visual Attention (TVA; Bundesen, 1990 Psychological...... afford an evolutionary advantage for an observer, ensuring that the most relevant objects are selected and encoded faster under high arousal, and making later processing more focused as the capacity of VSTM is decreased....

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

    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)

  1. Myocardial ischemia and angina pectoris

    Ambulatory monitoring of ST segment changes was performed in 60 patients presenting with angina, positive ECG stress tests and coronary artery disease, 85% of ischemic ECG events were asymptomatic, 37% occurred with no increase in heart rate and 15% of episodes either lasted 20 minutes or more or fluctuated in severity. A controlled pilot study in ten patients showed depression. Radionuclide studies in 50 patients with angina and coronary artery disease have shown that stress (i.e., atrial pacing) produced different patterns of disturbed regional myocardial perfusion related to the patient's exercise capacity and eventually leading to a decrease in regional myocardial perfusion during the ischemic episode. ST segment depression appeared only after the decrease in regional myocardial perfusion. These findings combined with past research suggest that patients with angina and coronary artery disease can suffer frequent asymptomatic disturbances of the regional myocardial perfusion. The frequency of these episodes and the time course for the recovery of the metabolic consequences mean that segments of ventricular myocardium may be constantly abnormal. The relative importance of changes in coronary tone and malfunction of platelets in the diseased coronary tree needs to be examined in clinical research. Pilot studies of antiplatelet agents have shown a significant beneficial effect on episodes of ischemia occurring at night and those occurring without any increase in heart rate. The techniques and observations in these patients with coronary artery disease all suggest that acute transient regional myocardial ischemia is caused by a variety of mechnisms. Further research using objective methods is required to discover the causes of ischemia and to rationalize treatment. (orig./MG)

  2. Myocardial ischemia in Kawasaki disease

    The detection of myocardial ischemia is essential for evaluation of patients with Kawasaki disease, especially who have had coronary artery lesions. To evaluate the clinical efficacy of Tl-201 single photon emission computed tomography (SPECT) after dipyridamole infusion (maximum dose 0.70 mg/kg) for detecting myocardial ischemia, 44 patients with Kawasaki disease aged 7.7±4.8 years at the study and 10 age matched controls were observed. In the Kawasaki disease group, significant coronary artery stenosis was observed in 14, coronary aneurysm without stenosis in 18, the regression of the coronary aneurysms in 2 and without coronary lesions in 10 patients. In 24 of 44 patients, treadmill exercise stress test was also performed at the same period. Myocardial ischemic changes were observed in 11 patients, all combined with significant coronary artery stenosis. The sensitivity of SPECT for detection of overall coronary stenosis was 79%, coronary that of treadmill exercise test was only 33% (p<0.001). Furthermore, among the patients having significant coronary stenosis, the severity score was significantly elevated in patients who had electrocardiographic abnormal Q wave compared to those without abnormal Q wave (51.0±38.8 versus 20.0±12.1, p<0.05). These data suggest that the pharmacological stress scintigraphy using dipyridamole injection provides not only the accurate detection but quantitative evaluation of myocardial ischemia in these patients. This noninvasive technique may become one of the most useful index for detection and follow-up of myocardial ischemia in Kawasaki disease. (author)

  3. Myocardial Noncompaction Presenting With Myocardial Bridge: A Case Report.

    Shen, Yuechun; Li, Xinchun; Lu, Dongfeng; Xiao, Aiyi; Li, Jun

    2015-09-01

    Myocardial noncompaction, namly isolated noncompaction of the left ventricular myocardium (NVM), is a rare congenital disease. It can be either seen in the absence of other cardiac anomalies, or associated with other congenital cardiac defects, mostly stenotic lesions of the left ventricular outflow tract. A myocardial bridge (MB) is thought being associated with coronary heart disease, such as coronary spasm, arrhythmia, and so on. The significance of MB in association with other congenital cardiac conditions is unknown.We report a novel case who was presented NVM and MB. A 34-year-old man complained of chest prickling-like pain and dizzy for 1 year. His blood pressure was 110/70 mm Hg. Echocardiograph revealed increased trabeculations below the level of papillary muscle of left ventricle (LV); deep intertrabecular recesses in the endocardial wall of LV particularly in apex free wall; and LV ejection fraction of 57%. A coronary computerized tomography scan showed that part, 38.9 cm, of left descending artery tunnel was surrounding by cardiac muscles rather than resting on top of the myocardium.The therapeutics interventions included lifestyle cares, agents of anti-ischemia and improvement myocardial cell metabolism. The patient was followed up for 2.6 years, and his general condition was stable.This case indicates that NVM can be developed with MB, and the complete diagnosis of NVM and MB should be made by different image studies. PMID:26356695

  4. A polymethoxy flavonoids-rich Citrus aurantium extract ameliorates ethanol-induced liver injury through modulation of AMPK and Nrf2-related signals in a binge drinking mouse model.

    Choi, Bong-Keun; Kim, Tae-Won; Lee, Dong-Ryung; Jung, Woon-Ha; Lim, Jong-Hwan; Jung, Ju-Young; Yang, Seung Hwan; Suh, Joo-Won

    2015-10-01

    Nobiletin and tangeretin are polymethoxy flavonoids (PMFs), found in rich quantities in the peel of citrus fruits. In the present study, we assessed the biological effect of the PMFs on liver damage using a mouse model of binge drinking. First, we extracted PMFs from the peels of Citrus aurantium to make Citrus aurantium extract (CAE). Male C57BL/6 mice were orally treated with silymarin and CAE (50, 100, and 200 mg/kg) for 3 days prior to ethanol (5 g/kg, total of 3 doses) oral gavage. Liver injury was observed in the ethanol alone group, as evidenced by increases in serum hepatic enzymes and histopathologic alteration, as well as by hepatic oxidative status disruption. CAE improved serum marker and hepatic structure and restored oxidative status by enhancing antioxidant enzyme levels and by reducing lipid peroxidation levels. In addition, CAE evidently suppressed inflammation and apoptosis in the livers of mice administered with ethanol, by 85% (tumor necrosis factor-α) and 44% compared to the control group, respectively. Furthermore, CAE activated lipid metabolism related signals and enhanced phosphorylation of AMP-activated protein kinase (AMPK) and nuclear factor E2-related factor 2 (Nrf2) with several cytoprotective proteins including heme oxygenase-1, NAD(P)H quinone oxidoreductase 1, and γ-glutamylcysteine synthetase. Taken together, the present study demonstrated that, CAE possesses antioxidant, anti-inflammatory, and antiapoptotic activity against ethanol-induced liver injury. PMID:26178909

  5. Assessment of myocardial viability using PET

    The potential for recovery of left ventricular dysfunction after myocardial revascularization represents a practical clinical definition for myocardial viability. The evaluation of viable myocardium in patients with severe global left ventricular dysfunction due to coronary artery disease and with regional dysfunction after acute myocardial infarction is an important issue whether left ventricular dysfunction may be reversible or irreversible after therapy. If the dysfunction is due to stunning or hibernation, functional improvement is observed. But stunned myocardium may recover of dysfunction with no revascularization. Hibernation is chronic process due to chronic reduction in the resting myocardial blood flow. There are two types of myocardial hibernation; 'functional hibernation' with preserved contractile reserve and 'structural hibernation' without contractile reserve in segments with preserved glucose metabolism. This review focus on the application of F-18 FDG and other radionuclides to evaluate myocardial viability. In addition the factors influencing predictive value of FDG imaging for evaluating viability and the different criteria for viability are also reviewed

  6. Reperfusion injury, stunning and myocardial viability

    Recent experimental data suggest that current thrombolytic strategies may not yet have achieved their full potential for myocardial salvage. In fact, reperfusion may result in microvascular and myocardial cellular injuries. These may translate into transient loss of contractile function ('myocardial stunning'), and possibly contribute to the ultimate extent of myocardial necrosis. The authors review current understanding about the significance, mechanisms, detection and possible treatment of phenomena following reperfusion. A number of imaging modalities, now available to detect the presence and amount of these dysfunctional but variable myocardial segments are presented. These include: Single Photon Emission Computed Tomography, Positron Emission Tomography and Dobutamine Stress Echocardiography. Myocardial reperfusion experiments using animal models have studied possible mechanisms responsible for reperfusion injury. These may help in the search for novel pharmacological and other adjunctive approaches which may-overcome potential adverse effects of reperfusion. 15 refs

  7. Depressive Symptoms Are Associated with Mental Stress-Induced Myocardial Ischemia after Acute Myocardial Infarction

    Jingkai Wei; Pratik Pimple; Shah, Amit J.; Cherie Rooks; Douglas Bremner, J.; Nye, Jonathon A.; Ijeoma Ibeanu; Nancy Murrah; Lucy Shallenberger; Paolo Raggi; Viola Vaccarino

    2014-01-01

    Objectives Depression is an adverse prognostic factor after an acute myocardial infarction (MI), and an increased propensity toward emotionally-driven myocardial ischemia may play a role. We aimed to examine the association between depressive symptoms and mental stress-induced myocardial ischemia in young survivors of an MI. Methods We studied 98 patients (49 women and 49 men) age 38–60 years who were hospitalized for acute MI in the previous 6 months. Patients underwent myocardial perfusion ...

  8. Anterior Myocardial Infarction Associated with Myocardial Bridging in a Young Man

    Ngow, HA; Wan Khairina, WMN

    2010-01-01

    A 43-year-old man presented with acute extensive anterior ST-segment elevation myocardial infarction. During coronary angiogram, a segment of myocardial bridging was noted in the mid-segment of left anteriordescending artery. The association of myocardial bridging and an anterior ST segment elevation is rarely reported in the medical literature. Myocardial bridging is caused by systolic compression of a coronary artery by overlying myocardium tissue. It is a rare coronary artery anomaly, whic...

  9. Kounis Syndrome together with Myocardial Bridging Leading to Acute Myocardial Infarction at Young Age

    Osman Karakaya; Murat Ugurlucan; Fatma Nihan Turhan Caglar; Ilker Murat Caglar; Alper Vural

    2011-01-01

    Kounis syndrome, also named as “allergic angina syndrome,” is a diagnosis in which exposure to an allergen causes mostly coronary spasm and rarely plaque rupture, resulting in ischemic myocardial events. Myocardial bridging is defined as an intramural segment of a coronary artery and its systolic compression by overlying fibers. Myocardial bridging generally has a benign prognosis and mostly affects the mid portion of left anterior descending coronary artery. However, some cases with myocardi...

  10. SERUM MAGNESIUM IN ACUTE MYOCARDIAL INFARCTION

    Nambakam Tanuja; Girish P

    2015-01-01

    BACKGROUND: In myocardial infarction, there occurs functional deficit of available magnesium due to trapping of free magnesium in adipocytes. Magnesium has been implicated in the pathogenesis of acute myocardial infarction and its complications. Magnesium ions are considered essential for the maintenance of functional integrity of myocardium. The serum magnesium concentration was found to have g reat significance in acute myocardial infarction. The present study was un...

  11. Leukocytosis: a risk factor for myocardial infarction

    Kotla SK

    2012-01-01

    Suman K KotlaDepartment of Internal Medicine, Memorial Medical Center, Johnstown, PA, USAAbstract: Myocardial infarction commonly results from atherosclerotic lesions in the coronary arteries. Approximately 5% of patients with acute myocardial infarction do not have atherosclerotic disease. In this case report, we present an unusual leukostatic complication in a patient with acute myeloblastic leukemia and extreme hyperleukocytosis who presented with an acute myocardial infarction that resolv...

  12. Acute myocardial involvement after heroin inhalation

    Ritu Karoli; Fatima, J.; Pushker Singh; Kazmi, Khursheed I.

    2012-01-01

    Amongst the illicit drugs cocaine, amphetamines and cannabis have been studied and documented well to cause myocardial infarction by different mechanisms but there is very sparse data available on myocardial involvement after heroin abuse. We report a young man who developed acute myocardial injury after heroin inhalation and alcohol binge drinking. Heroin induced cardio toxic effect and vasospasm compounded by alcohol were suspected to be the cause of this.

  13. Clinical Practice Guidelines for Acute Myocardial Infarction.

    Francisco de Jesús Valladares Carvajal; Arelys Falcón Hernández; Félix Rolando Jorrín Román; Juan Emilio García Rivas

    2009-01-01

    Clinical Practice Guidelines for Acute Myocardial Infarction. It has been defined as the clinical condition caused by the ischemic myocardial necrosis, usually caused by abrupt reduction of coronary blood irrigation affecting one or more myocardial areas. The document includes a review and update of the concept, classification, diagnosis and therapy. Risk stratification and main aspects of rehabilitation are also stressed. It includes assessment guidelines focused on the most important aspect...

  14. Acute myocardial involvement after heroin inhalation

    Ritu Karoli

    2012-01-01

    Full Text Available Amongst the illicit drugs cocaine, amphetamines and cannabis have been studied and documented well to cause myocardial infarction by different mechanisms but there is very sparse data available on myocardial involvement after heroin abuse. We report a young man who developed acute myocardial injury after heroin inhalation and alcohol binge drinking. Heroin induced cardio toxic effect and vasospasm compounded by alcohol were suspected to be the cause of this.

  15. Clinical Practice Guidelines for Acute Myocardial Infarction.

    Francisco De Jesús Valladares Carvajal

    2009-03-01

    Full Text Available Clinical Practice Guidelines for Acute Myocardial Infarction. It has been defined as the clinical condition caused by the ischemic myocardial necrosis, usually caused by abrupt reduction of coronary blood irrigation affecting one or more myocardial areas. The document includes a review and update of the concept, classification, diagnosis and therapy. Risk stratification and main aspects of rehabilitation are also stressed. It includes assessment guidelines focused on the most important aspects to be accomplished.

  16. Myocardial tissue tagging with cardiovascular magnetic resonance

    Bluemke David A; Osman Nael F; Cheng Susan; Shehata Monda L; Lima João AC

    2009-01-01

    Abstract Cardiovascular magnetic resonance (CMR) is currently the gold standard for assessing both global and regional myocardial function. New tools for quantifying regional function have been recently developed to characterize early myocardial dysfunction in order to improve the identification and management of individuals at risk for heart failure. Of particular interest is CMR myocardial tagging, a non-invasive technique for assessing regional function that provides a detailed and compreh...

  17. Myocardial infarction and subsequent pregnancy

    Tedoldi Citânia Lúcia

    2000-01-01

    Full Text Available We report the case of a 40-year-old woman with 2 previous myocardial infarctions, revascularization surgery, and an ongoing pregnancy complicated with preeclampsia and fetal hypoxia. Her follow-up performed by a multidisciplinary team made possible the birth through cesarean section of a premature infant of the female sex with a very low birth weight, but without severe respiratory distress of the hyaline membrane disease type. Three months after the delivery, mother and daughter were healthy.

  18. Enteroviruses in Acute Myocardial Infarction

    A Gholoobi; MS Nabavinia; T Mohamadpoor; MS Alavi; Z Meshkat

    2012-01-01

    Background: Human enteroviruses (EVs) may have a role as a possible risk factor in the pathogenesis of MI. The aim of this study was to evaluate the presence of enterovirus genomic RNA in peripheral blood samples of patients with acute myocardial infarction (MI). Methods: We investigated the presence of enterovirus genomic RNA in the peripheral blood of 115 patients with acute MI hospitalized in the Coronary Care Unit of Imam Reza and Ghaem University Hospitals (Mashhad, Iran) by RT-PCR using...

  19. ANGIOGRAPHIC ASPECTS OF MYOCARDIAL BRIDGES

    Sujatha M; V Subhadra Devi; C. S. S. Raju; B. Yugandhar; Nagaraju

    2015-01-01

    Introduction: The segment of epicardial coronary artery that traverses intramurally through the myocardium and bridged by a bunch of cardiac muscle fibers is called tunneled artery or intramural artery. The band of cardiac muscle fibers passing over the tunneled artery segment is named as myocardial bridge. During angiography milking effect is observed during systole due to the external pressure of muscle fibers on the tunneled artery that leads to narrowing of vessel lumen and further isc...

  20. Ventricular Stimulation After Myocardial Infarction

    Béatrice Brembilla-Perrot

    2011-01-01

    Ventricular stimulation after myocardial infarction (MI) is still recommended (class IB) in patients with syncope and left ventricular ejection fraction (LVEF) more than 30-35%, in asymptomatic patients with a LVEF between 30-40% and with non sustained ventricular tachycardia (VT) patients at Holter monitoring. It can also identify patients at high risk of arrhythmic events in the early post-MI period. Combined with imaging methods PVS could be widely used again during VT ablation.

  1. The Orchestra of Myocardial Regeneration

    Siddiqi, S

    2014-01-01

    A glimpse on previous and current literature ignites the recognition of the luxurious era that cardiac science has reached. In particular, the past fifteen years have provided tremendous advancements in the field of myocardial biology with the characterization of cardiac stem cells, reprogramming of somatic cells, microRNA discovery, exosome-protocols and imaging modalities. In addition, conventional and outdated biological processes such as myocyte metabolism, cell cycle, and senescence are ...

  2. Myocardial bridging as a cause of acute myocardial infarction: a case report

    Emiroglu Yunus

    2002-09-01

    Full Text Available Abstract Background Systolic compression of a coronary artery by overlying myocardial tissue is termed myocardial bridging. Myocardial bridging usually has a benign prognosis, but some cases resulting in myocardial ischemia, infarction and sudden cardiac death have been reported. We are reporting a case of myocardial bridging which was complicated with acute myocardial infarction associated with inappropriate blood donation. Case presentation A 33 year-old-man was admitted to our emergency with acute anteroseptal myocardial infarction after a blood donation. The electrocardiography showed sinus rhythm and was consistent with an acute anteroseptal myocardial infarction. We decided to perform primary percutanous intervention (PCI. Myocardial bridging was observed in the mid segment of the left anterior descending coronary artery on coronary angiogram. PCI was canceled and medical follow up was decided. Blood transfusion was made because he had a deep anemia. A normal hemaglobin level and clinical reperfusion was achieved after ten hours by blood transfusion. At the one year follow up visit, our patient was healthy and had no cardiac complaints. Conclusions Myocardial bridging may cause acute myocardial infarction in various clinical conditions. Although the condition in this case caused profound anemia related acute myocardial infarction, its treatment and management was unusual.

  3. Power, Social Identity and Fashion Consumption : A thesis on how female executives use power-coded dressing as a tool to accentuate power as a part of their social identity.

    Ordonez Asenjo, Carolina

    2014-01-01

    The aim of the thesis is to contribute to the CCT research field on social identity, by placing a focus on power from a customer perspective and studying how power can be accentuated within social identity. Theory from CCT with a focus on social identity has been used in combination with extensive literature on power and authority from a sociological perspective and literature from Fashion-Studies focusing on power-dressing, conspicuous consumption and luxury. The research question is: How is...

  4. Cardiac MRI for myocardial ischemia.

    Daly, Caroline

    2013-01-01

    Proper assessment of the physiologic impact of coronary artery stenosis on the LV myocardium can affect patient prognosis and treatment decisions. Cardiac magnetic resonance imaging (CMR) assesses myocardial perfusion by imaging the myocardium during a first-pass transit of an intravenous gadolinium bolus, with spatial and temporal resolution substantially higher than nuclear myocardial perfusion imaging. Coupled with late gadolinium enhancement (LGE) imaging for infarction during the same imaging session, CMR with vasodilating stress perfusion imaging can qualitatively and quantitatively assess the myocardial extent of hypoperfusion from coronary stenosis independent of infarcted myocardium. This approach has been validated experimentally, and multiple clinical trials have established its diagnostic robustness when compared to stress single-photon emission computed tomography. In specialized centers, dobutamine stress CMR has been shown to have incremental diagnostic value above stress echocardiography due to its high imaging quality and ability to image the heart with no restriction of imaging window. This paper reviews the technical aspects, diagnostic utility, prognostic values, challenges to clinical adaptation, and future developments of stress CMR imaging.

  5. Myocardial ischaemia during tracheal intubation and extubation.

    Edwards, N D; Alford, A M; Dobson, P M; Peacock, J E; Reilly, C S

    1994-10-01

    The incidence of myocardial ischaemia during tracheal intubation and extubation was compared using ambulatory ECG monitoring in 60 patients undergoing a variety of different surgical operations. Seven patients had myocardial ischaemia after tracheal intubation and seven patients during tracheal extubation. The patients who developed myocardial ischaemia during tracheal extubation had significantly greater rate-pressure products immediately before tracheal extubation (P < 0.05) and 1 min after tracheal extubation (P < 0.01) compared with those patients who did not develop myocardial ischaemia during extubation. PMID:7999498

  6. Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction

    Joshi, Nikhil V; Toor, Iqbal; Shah, Anoop S V; Carruthers, Kathryn; Alex T. Vesey; Alam, Shirjel R; Sills, Andrew; Hoo, Teng Y; Melville, Adam J; Langlands, Sarah P; Jenkins, William S A; Uren, Neal G; Mills, Nicholas L.; Fletcher, Alison M; van Beek, Edwin J.R.

    2015-01-01

    BACKGROUND: Preclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.METHODS AND RESULTS: Overall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonv...

  7. Thrombolysis significantly reduces transient myocardial ischaemia following first acute myocardial infarction

    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...... less than 0.02). Thrombolysis resulted in a non-significant reduction in exercise-induced ST segment depression: prevalence 43% vs 62% in controls. However, during ambulatory monitoring the duration of transient myocardial ischaemia was significantly reduced in thrombolysed patients: 322 min vs 1144...... myocardial ischaemia. This may explain the improvement in myocardial function during physical activities, which was also observed in this study....

  8. Screening for silent myocardial ischemia caseof diabetics : interest of myocardial perfusion scintigraphy

    Silent myocardial ischemia is a major cause of morbidity and mortality in diabetic patients. Its diagnosis by noninvasive means such as myocardial SPECT would improve the management of these patients. The purpose of this study is to assess the frequency of silent myocardial ischemia in asymptomatic diabetics and their evolution. As a result, the myocardial SPECT is a reliable tool for screening for silent myocardial ischemia in diabetic patients. Its prognostic value allows to stratify the cardiac risk and guide therapeutic management. Its integration into a screening strategy in Tunisia seems limited by its low availability and cost. The latter could be reduced by better patient selection.

  9. Comparison of dobutamine stress echocardiography with exercise reinjection thallium myocardial perfusion scan to detect myocardial cell viability

    A comparison of dobutamine stress echocardiography with exercise reinjection thallium myocardial perfusion scan on known coronary artery disease patients for detection of myocardial cell viability is given

  10. Do episodes of anger trigger myocardial infarction?

    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....

  11. [Fibrinolysis in acute myocardial infarct].

    Bleifeld, W

    1987-10-24

    Fibrinolysis has opened up a new avenue in the treatment of acute myocardial infarction (AMI). In principle, the rate of reperfusion depends on the type of compound used, the mode of administration and the time between onset of symptoms and the beginning of treatment. With intracoronary streptokinase the reperfusion rate is of the order of 85%. Intravenous urokinase administered as a bolus results in a reopening rate of 50-60%; a similar rate of reperfusion is achieved with rt-PA as infusion, while i.v. streptokinase produces about 50% reopened coronary vessels. The final infarct size is decreased in 70% of patients if fibrinolysis is initiated within 2.5 hours after the onset of symptoms and followed by reopening of the occluded vessel. This results in a lowering of in-hospital mortality, which in various studies is of the order of 45-60%.- Bearing in mind the contraindications, fibrinolysis should be initiated within 3 hours. Hemodynamic improvement by a decrease of infarct size may also be achieved beyond 3 hours in large anterior myocardial infarctions and in posterior infarctions with cardiogenic shock. Early initiation of thrombolysis is of major importance in improving left ventricular function and lowering mortality following acute myocardial infarction. Therefore, prehospital thrombolytic therapy should be considered. - In the postinfarction phase coronary angiography is indicated in patients with angina at rest, stable angina of ECG signs of ischemia. In this situation transfer to a specialized cardiology division for possible percutaneous transluminal angioplasty is indicated. - Reocclusion after successful thrombolysis occurs in 20-30%, and it is therefore important to avoid reinfarction to improve the long term prognosis after AMI.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:3321420

  12. Myocardial infarction and nocturnal hypoxaemia

    Penčić Biljana

    2007-01-01

    Full Text Available Introduction: There is an increased risk of cardiovascular morbidity and mortality in patients with nocturnal intermittent hypoxaemia. Objecive. The aim of this study was to evalute the influence of nocturnal hypoxaemia on ventricular arrhythmias and myocardial ischaemia in patients with myocardial infarction (MI. Method. We studied 77 patients (55.8±7.9 years with MI free of complications, chronic pulmonary diseases, abnormal awake blood gases tension. All patients underwent overnight pulse oximetry and 24-hour electrocardiography. Patients were divided into two groups according to nocturnal hypoxaemia. Total number of ventricular premature complex (VPC; maximal VPC/h; incidence of VPC Lown class>2 and occurrence of ST-segment depression were analyzed for nocturnal (10 PM to 6 AM, daytime (6 AM to 22 PM periods and for the entire 24 hours. Results. Both groups were similar in age, gender, standard risk factors, myocardial infarction size and did not differ in VPC during the analyzed periods. The number of nocturnal maximal VPC/h was insignificantly greater in group 1 (with hypoxaemia compared to group 2 (without hypoxaemia, (p=0.084. Maximal VPC/h did not differ significantly either for daytime or for 24 hours among the groups. Nocturnal VPC Lown>2 were significantly more frequent in group 1 (25% vs 0%, p=0.002. The incidence of VPC Lown>2 was similar during the daytime, and during 24 hrs in both groups. Occurrence of ST-segment depression did not differ between groups 1 and 2. Conclusion. Nocturnal hypoxaemia was associated with complex nocturnal ventricular arrhythmias in patients with MI. .

  13. Solar activity and myocardial infarction.

    Szczeklik, E; Mergentaler, J; Kotlarek-Haus, S; Kuliszkiewicz-Janus, M; Kucharczyk, J; Janus, W

    1983-01-01

    The correlation between the incidence of myocardial infarction, sudden cardiac death, the solar activity and geomagnetism in the period 1969-1976 was studied, basing on Wrocław hospitals material registered according to WHO standards; sudden death was assumed when a person died within 24 hours after the onset of the disease. The highest number of infarctions and sudden deaths was detected for 1975, which coincided with the lowest solar activity, and the lowest one for the years 1969-1970 coinciding with the highest solar activity. Such an inverse, statistically significant correlation was not found to exist between the studied biological phenomena and geomagnetism. PMID:6851574

  14. Circadian influences on myocardial infarction.

    Virag, Jitka A I; Lust, Robert M

    2014-01-01

    Components of circadian rhythm maintenance, or "clock genes," are endogenous entrainable oscillations of about 24 h that regulate biological processes and are found in the suprachaismatic nucleus (SCN) and many peripheral tissues, including the heart. They are influenced by external cues, or Zeitgebers, such as light and heat, and can influence such diverse phenomena as cytokine expression immune cells, metabolic activity of cardiac myocytes, and vasodilator regulation by vascular endothelial cells. While it is known that the central master clock in the SCN synchronizes peripheral physiologic rhythms, the mechanisms by which the information is transmitted are complex and may include hormonal, metabolic, and neuronal inputs. Whether circadian patterns are causally related to the observed periodicity of events, or whether they are simply epi-phenomena is not well established, but a few studies suggest that the circadian effects likely are real in their impact on myocardial infarct incidence. Cycle disturbances may be harbingers of predisposition and subsequent response to acute and chronic cardiac injury, and identifying the complex interactions of circadian rhythms and myocardial infarction may provide insights into possible preventative and therapeutic strategies for susceptible populations. PMID:25400588

  15. Contemporaryperspective on endogenous myocardial regeneration

    2015-01-01

    Considering the complex nature of the adult heart,it is no wonder that innate regenerative processes,while maintaining adequate cardiac function, fall shortin myocardial jeopardy. In spite of these enchaining limitations, cardiac rejuvenation occurs as well asrestricted regeneration. In this review, the backgroundas well as potential mechanisms of endogenousmyocardial regeneration are summarized. We presentand analyze the available evidence in three subsequentsteps. First, we examine the experimental researchdata that provide insights into the mechanisms andorigins of the replicating cardiac myocytes, includingcell populations referred to as cardiac progenitor cells(i.e. , c-kit+ cells). Second, we describe the role ofclinical settings such as acute or chronic myocardialischemia, as initiators of pathways of endogenousmyocardial regeneration. Third, the hitherto conductedclinical studies that examined different approachesof initiating endogenous myocardial regeneration infailing human hearts are analyzed. In conclusion, wepresent the evidence in support of the notion thatregaining cardiac function beyond cellular replacementof dysfunctional myocardium via initiation of innateregenerative pathways could create a new perspectiveand a paradigm change in heart failure therapeutics.Reinitiating cardiac morphogenesis by reintroducingdevelopmental pathways in the adult failing heart mightprovide a feasible way of tissue regeneration. Basedon our hypothesis "embryonic recall", we present firstsupporting evidence on regenerative impulses in themyocardium, as induced by developmental processes.

  16. New imaging techniques in myocardial perfusion SPECT

    Gated myocardial SPECT and attenuation correction gave birth to new insights into the pathophysiology of ischemic myocardial perfusion and function in clinical routine practice. Gated myocardial Tc-99m-compound SPECT improved diagnostic accuracy of coronary artery disease and enabled us to observe motion and thickening of myocardial walls as well as myocardial perfusion at the same time. Quantitative and qualitative assessment of myocardial performance and perfusion let us to understand the myocardial physiology in ischemia and infarction. In every patient who underwent gated perfusion SPECT, we will find ejection fraction, left ventricular volumes and regional wall motion. There are hopes to use gated Tl-201 SPECT for the same purpose and to use gated SPECT for evaluation of wall motion and thickening at stress or immediate post-stress. Attenuation correction could improve diagnostic accuracy mainly by increasing normalcy ratio or performance of non-expert physicians Both gated methods and attenuation correction improved specificity of non-expert physicians in diagnosing patients with moderate pretest likelihood. New imaging techniques will fill the desire of cardiologists to examine function and perfusion, and possibly metabolism in their clinical routine practice

  17. Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction by Biomarkers

    2016-01-25

    Acute Myocardial Infarction (AMI); Acute Coronary Syndrome (ACS); ST Elevation (STEMI) Myocardial Infarction; Ischemic Reperfusion Injury; Non-ST Elevation (NSTEMI) Myocardial Infarction; Angina, Unstable

  18. Clinical Characteristics and Outcomes of Patients with Myocardial Infarction, Myocardial Injury, and Nonelevated Troponins

    Sarkisian, Laura; Saaby, Lotte; Poulsen, Tina S; Gerke, Oke; Jangaard, Nikolaj; Hosbond, Susanne; Diederichsen, Axel C P; Thygesen, Kristian; Mickley, Hans

    2016-01-01

    troponin value is encountered in the absence of obvious myocardial ischemia, a careful search for other clinical conditions is crucial. METHODS: In 2010 to 2011, we prospectively studied hospitalized patients who had cardiac troponin I measured on clinical indication. An acute myocardial infarction was...... values ≤30 ng/L were classified as nonelevated cardiac troponin I. Follow-up was at least 3 years with all-cause mortality as the sole clinical end point. RESULTS: A total of 3762 patients were included. Of these, 488 (13%) had acute myocardial infarction, 1089 (29%) had myocardial injury, and 2185 (58......%, respectively). CONCLUSIONS: Patients with myocardial injury are older and have more comorbidity than those with acute myocardial infarction. Both groups exhibit a poorer prognosis than patients with nonelevated cardiac troponin I values. Of note, a very high long-term mortality is observed in patients with...

  19. Insulin-Like Growth Factor-1 Preconditioning Accentuates Intrinsic Survival Mechanism in Stem Cells to Resist Ischemic Injury by Orchestrating Protein Kinase Cα–Erk1/2 Activation

    Lu, Gang; Ashraf,Muhammad; Haider, Khawaja Husnain

    2012-01-01

    Aims: To test our hypothesis that the intrinsic molecular mechanism in stem cells for adaptation to ischemia is accentuated by preconditioning with insulin-like growth factor (IGF-1). Results: Bone marrow Sca-1+ cells were exposed to oxygen and glucose deprivation (OGD) for up to 12 h. Erk1/2 was activated in Sca-1+ cells under OGD which was blocked by MEK inhibitor (PD98059) and resulted in accelerated cell death. Moreover, elevated intracellular calcium with concomitant activation of protei...

  20. Autophagy and ethanol-induced liver injury

    Terrence M Donohue Jr

    2009-01-01

    The majority of ethanol metabolism occurs in the liver. Consequently, this organ sustains the greatest damage from ethanol abuse. Ethanol consumption disturbs the delicate balance of protein homeostasis in the liver, causing intracellular protein accumulation due to a disruption of hepatic protein catabolism.Evidence indicates that ethanol or its metabolism impairs trafficking events in the liver, including the process of macroautophagy, which is the engulfment and degradation of cytoplasmic constituents by the lysosomal system. Autophagy is an essential, ongoing cellular process that is highly regulated by nutrients,endocrine factors and signaling pathways. A great number of the genes and gene products that govern the autophagic response have been characterized and the major metabolic and signaling pathways that activate or suppress autophagy have been identified. This review describes the process of autophagy, its regulation and the possible mechanisms by which ethanol disrupts the process of autophagic degradation. The implications of autophagic suppression are discussed in relation to the pathogenesis of alcohol-induced liver injury.

  1. Ethanol Induced Shortening of DNA in Nanochannels

    Gemmen, Greg; Reisner, Walter; Tegenfeldt, Jonas; Linke, Heiner

    2010-03-01

    The confinement of DNA in nanochannels has greatly facilitated the study of DNA polymer physics and holds promise as a powerful tool for genomic sequencing. Ethanol precipitation of DNA is a common tool in molecular biology, typically in >70% [EtOH]. Even at lower ethanol concentrations, however, DNA transforms from B-form to A-form, a shorter yet slightly less twisted conformation. Accordingly, we isolated individual YOYO-1 labeled λ-DNA molecules in 100nmx100nm channels in 0, 20, 40 and 60% [EtOH]. We observed a dramatic shortening in the mean measured lengths with increasing [EtOH] and a broadening of the distribution of measured lengths at the intermediate concentrations. These observed lengths are less than those expected from fully A-form λ-DNA, suggesting that poor solvency effects are involved. Also, substantial spatial variations in intensity in a small number of molecules at the higher [EtOH] suggest the presence of higher order DNA conformations, in accord with the observation that the effective persistence length of DNA has been greatly reduced.

  2. Nitroglycerine Induced Acute Myocardial Infarction in a Patient with Myocardial Bridging

    Dragana Rujic; Mette Lundgren Nielsen; Karsten Tange Veien; Manan Pareek

    2014-01-01

    Muscle overlying an intramyocardial segment of a coronary artery is termed a myocardial bridge. The intramyocardial segment, the tunneled artery, is compressed during systole. The condition is generally benign but may occasionally cause myocardial ischemia, infarction, arrhythmia, or sudden cardiac death. We present a case regarding a 52-year-old man with exercise-induced angina who was diagnosed with a myocardial bridge overlying the left anterior descending artery. He was initially treated ...

  3. Histochemical and immunohistochemical analyses of the myocardial scar fallowing acute myocardial infarction

    Tatić Vujadin; Rafajlovski Sašo; Kanjuh Vladimir; Gajanin Radoslav; Suščević Dušan; Balint Bela; Obradović Slobodan

    2012-01-01

    Background/Aim. The heart has traditionally been considered as a static organ without capacity of regeneration after trauma. Currently, the more and more often asked question is whether the heart has any intrinsic capacities to regenerate myocytes after myocardial infarction. The aim of this study was to present the existence of the preserved muscle fibers in the myocardial scar following myocardial infarction as well as the presence of numerous cells of various size and form that diffe...

  4. Comparative study on the localization of myocardial ischemia by myocardial perfusion SPECT and exercise electrocardiography

    Objective: To investigate the correspondence between the myocardial perfusion SPECT and exercise electrocardiography (ECG) in localization of myocardial ischemia. Methods: Three hundred and two patients with abnormal findings in the myocardial perfusion SPECT and ECG were selected and Chi-square test was performed to analyze the relationship between ECG and SPECT in determining the ischemic myocardial segment. Results: Compared with patients with ST depression, most patients with ST elevation had significantly more angina symptoms in history occurring during exercise test, and lower exercise tolerability (P<0.05). Some weak correspondence (K=0.36, P<0.01) was shown between the localization of ST depression and defect territory of myocardial perfusion, while a complete correspondence (K=1.00, P<0.01) between ST elevation and SPECT in determining the abnormal myocardial segment was observed. In patients with anterior ST depression, perfusion defects occurred more frequently in left anterior descending coronary artery (LAD) territory (66.9%) than in right coronary artery (RCA) territory (33.1%). ST segment depression related poorly with the results of myocardial perfusion in determining the defects. Conclusion: The exercise-induced ST elevation is more correspondent to the defects of myocardial perfusion in the localization of myocardial ischemia compared with ST depression

  5. SPECT Myocardial Blood Flow Quantitation Concludes Equivocal Myocardial Perfusion SPECT Studies to Increase Diagnostic Benefits.

    Chen, Lung-Ching; Lin, Chih-Yuan; Chen, Ing-Jou; Ku, Chi-Tai; Chen, Yen-Kung; Hsu, Bailing

    2016-01-01

    Recently, myocardial blood flow quantitation with dynamic SPECT/CT has been reported to enhance the detection of coronary artery disease in human. This advance has created important clinical applications to coronary artery disease diagnosis and management for areas where myocardial perfusion PET tracers are not available. We present 2 clinical cases that undergone a combined test of 1-day rest/dipyridamole-stress dynamic SPECT and ECG-gated myocardial perfusion SPECT scans using an integrated imaging protocol and demonstrate that flow parameters are capable to conclude equivocal myocardial perfusion SPECT studies, therefore increasing diagnostic benefits to add value in making clinical decisions. PMID:26053731

  6. The clinical application value of myocardial perfusion imaging in evaluating coronary artery myocardial bridge patients with symptoms

    Objective: Myocardial bridge is a common inborn coronary artery anomaly, myocardial bridge may be associated with myocardial ischemia. Only a few patients with coronary artery myocardial bridge were evaluated with nuclear medicine techniques. The aim of this study was to investigate the role of nuclear cardiology with myocardial perfusion technique in symptomatic myocardial bridge patients. Methods Nineteen myocardial bridge patients with the symptoms of chest pain and chest distress were analyzed retrospectively. 99Tcm-methoxyisobutylisonitrile (MIBI) myocardial perfusion images (both exercise and rest) were performed in all. Imaging results were compared with the results of movement electrocardiogram (ECG) and coronary arteriography. The t test or χ2 test was used to statistically analyze the data with Stata 7.0 software. Results: Of the 19 patients, 18 patients had myocardial bridge locating at the left anterior descending artery, 1 patient at the left anterior descending and left circumflex artery, the mean angiographic systolic occlusion within the myocardial bridge was (65.4 ± 22.1)%. Of these 19 patients, Exercise-rest 99Tcm-MIBI myocardial perfusion imaging defined positive myocardial ischemia in 10 and negative in 9 patients. Of the 10 patients with 99Tcm-MIBI myocardial perfusion imaging defined myocardial ischemia, 8 had reversible radioactive defect of partial anterior wall and (or) apex, 1 had reversible defect of post lateral wall and post septal wall, and 1 had reversible defect of inferior wall. The positive predictive value of myocardial perfusion imaging was 52.6% (10/19), which was higher than movement ECG [21.1% (4/19), χ2= 4.07, P 99Tcm-MIBI myocardial periusion imaging defined myocardial ischemia. Six cases with Grade II stenosis, two were 99Tcm-MIBI myocardial perfusion imaging defined myocardial ischemia. Eight cases with Grade III stenosis, seven were 99Tcm-MIBI myocardial perfusion imaging defined myocardial ischemia. The mean angio

  7. The Effects of Combined Adiponectin-Metformin on Glucose and Lipids Levels in Mice and Acute Toxicity and Anti-Ulcerogenic Activity of Adiponectin Against Ethanol-Induced Gastric Mucosal Injuries in Rat

    Mohammed A. Alshawsh

    2011-11-01

    Full Text Available Adiponectin is a protein hormone secreted entirely by abdominal fat tissue. It exhibits various biological activities. The present study was performed to evaluate the effects of metformin alone or in combination with adiponectin on blood glucose, TG (triglyceride, CHOL (Total cholesterol, LDL (Low density lipoprotein and HDL (High density lipoprotein levels in mice and also to evaluate the anti-ulcerogenic activity of adiponectin against ethanol induced gastric mucosal injury in rats. Three groups of mice were gavaged with 1% volume/body weight high fat-sucrose. Metformin at a dosage of 250 mg/kg was added to the feed and a dosage of 2.5 mg/kg adiponectin was injected intraperitoneally (i.p. Blood glucose was measured at one hour intervals for five hours. Blood concentrations of TG, CHOL, LDL and HDL were also measured at the end of the fifth hour of the experiment. On the other hand, four groups of adult healthy rats were i.p. injected with distilled water, omeprazole 20 mg/kg, 2.5 mg/kg and 5 mg/kg adiponectin one hour before oral administration of absolute ethanol to generate gastric mucosal injury. After an additional hour the rats were sacrificed and the ulcer areas of the gastric walls were determined. Furthermore, an acute toxicity study has indicated no mortality with 5 mg/kg dose of adiponectin injected i.p in rats and no major clinical signs of toxicity were observed. The results indicate that the effect of a combination of metformin and adiponectin on blood glucose and HDL is quite effective. Histology of the gastric wall of negative control rats revealed severe damage of gastric mucosa, along with edema and leucocyte infiltration of the submucosal layer compared to rats pre-treated with either omeprazole or adiponectin extract where there was marked gastric protection along with reduction or inhibition of edema and leucocytes infiltration. The results suggest that combination of metfomin and adiponectin give a promising antidiabetic

  8. Experimental myocardial ischemia. Pt. 2

    The comparative effects of meglumine sodium diatrizoate (MSD), sodium meglumine calcium metrizoate (SMCM), and metrizamide (M) were studied in an isolated canine heart preparation. The parameters observed were coronary blood flow (CBF), myocardial contractile force (MCF), positive and negative dF/dt, and perfusion pressure during normal and ischemic perfusion conditions. MSD had an initial negative inotropic effect but baseline MCF returned in 1 min during normal perfusion and 2 min under ischemic conditions. SMCM and M had only a positive inotropic effect under normal perfusion. However, during ischemia, the positive effect of SMCM was followed by a decrease in contractile force. M showed only a positive effect on force during ischemia. Our results indicate that calcium additive may increase the risk of coronary arteriography in patients with severe coronary artery disease. (orig.)

  9. Repetitive myocardial infarctions secondary to delirium tremens.

    Schwartzberg, David; Shiroff, Adam

    2014-01-01

    Delirium tremens develops in a minority of patients undergoing acute alcohol withdrawal; however, that minority is vulnerable to significant morbidity and mortality. Historically, benzodiazepines are given intravenously to control withdrawal symptoms, although occasionally a more substantial medication is needed to prevent the devastating effects of delirium tremens, that is, propofol. We report a trauma patient who required propofol sedation for delirium tremens that was refractory to benzodiazepine treatment. Extubed prematurely, he suffered a non-ST segment myocardial infarction followed by an ST segment myocardial infarction requiring multiple interventions by cardiology. We hypothesize that his myocardial ischemia was secondary to an increased myocardial oxygen demand that occurred during his stress-induced catecholamine surge during the time he was undertreated for delirium tremens. This advocates for the use of propofol for refractory benzodiazepine treatment of delirium tremens and adds to the literature on the instability patients experience during withdrawal. PMID:25197580

  10. Myocardial hypoperfusion on conventional contrast computed tomography.

    Ching, Shing; Chung, Tak Shun

    2015-10-01

    Non–electrocardiogram (ECG)–gated contrast computed tomography (CT) is commonly performed to exclude aortic dissection in chest pain patients. Besides evaluating the aorta for dissection flap, attention should be paid to the myocardium for areas of hypoenhancement that may suggest ischemia. Current models of multidetector CT enable assessment of myocardial perfusion with minimal motion artifact even without ECG gating. Transmural hypoenhancement with preserved wall thickness in a coronary distribution is highly specific for acute myocardial infarction. We report 2 cases of acute chest pain with initial nondiagnostic studies that underwent CT aortogram to exclude dissection. Instead, the CT showed myocardial hypoenhancement in left anterior descending artery territory. Myocardial hypoenhancement occurred before ST-segment elevation on ECG, suggesting that recognition of this important finding may lead to earlier revascularization decisions. PMID:26321167