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Sample records for acute pulmonary inflammation

  1. Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation

    Silvie Kremserova

    2016-01-01

    Full Text Available Systemic inflammation accompanying diseases such as sepsis affects primarily lungs and induces their failure. This remains the most common cause of sepsis induced mortality. While neutrophils play a key role in pulmonary failure, the mechanisms remain incompletely characterized. We report that myeloperoxidase (MPO, abundant enzyme in neutrophil granules, modulates the course of acute pulmonary inflammatory responses induced by intranasal application of lipopolysaccharide. MPO deficient mice had significantly increased numbers of airway infiltrated neutrophils compared to wild-type mice during the whole course of lung inflammation. This was accompanied by higher levels of RANTES in bronchoalveolar lavage fluid from the MPO deficient mice. Other markers of lung injury and inflammation, which contribute to recruitment of neutrophils into the inflamed lungs, including total protein and other selected proinflammatory cytokines did not significantly differ in bronchoalveolar lavage fluid from the wild-type and the MPO deficient mice. Interestingly, MPO deficient neutrophils revealed a decreased rate of cell death characterized by phosphatidylserine surface expression. Collectively, the importance of MPO in regulation of pulmonary inflammation, independent of its putative microbicidal functions, can be potentially linked to MPO ability to modulate the life span of neutrophils and to affect accumulation of chemotactic factors at the inflammatory site.

  2. Lung Neutrophilia in Myeloperoxidase Deficient Mice during the Course of Acute Pulmonary Inflammation.

    Kremserova, Silvie; Perecko, Tomas; Soucek, Karel; Klinke, Anna; Baldus, Stephan; Eiserich, Jason P; Kubala, Lukas

    2016-01-01

    Systemic inflammation accompanying diseases such as sepsis affects primarily lungs and induces their failure. This remains the most common cause of sepsis induced mortality. While neutrophils play a key role in pulmonary failure, the mechanisms remain incompletely characterized. We report that myeloperoxidase (MPO), abundant enzyme in neutrophil granules, modulates the course of acute pulmonary inflammatory responses induced by intranasal application of lipopolysaccharide. MPO deficient mice had significantly increased numbers of airway infiltrated neutrophils compared to wild-type mice during the whole course of lung inflammation. This was accompanied by higher levels of RANTES in bronchoalveolar lavage fluid from the MPO deficient mice. Other markers of lung injury and inflammation, which contribute to recruitment of neutrophils into the inflamed lungs, including total protein and other selected proinflammatory cytokines did not significantly differ in bronchoalveolar lavage fluid from the wild-type and the MPO deficient mice. Interestingly, MPO deficient neutrophils revealed a decreased rate of cell death characterized by phosphatidylserine surface expression. Collectively, the importance of MPO in regulation of pulmonary inflammation, independent of its putative microbicidal functions, can be potentially linked to MPO ability to modulate the life span of neutrophils and to affect accumulation of chemotactic factors at the inflammatory site. PMID:26998194

  3. Alveolar recruitment of ficolin-3 in response to acute pulmonary inflammation in humans

    Plovsing, Ronni R; Berg, Ronan M G; Munthe-Fog, Lea;

    2016-01-01

    BACKGROUND: Ficolins serve as soluble recognition molecules in the lectin pathway of complement. They are known to participate in the systemic host-response to infection but their role in local pulmonary defence is still incompletely understood. The purpose of this study was to clarify whether...... acute lung and systemic inflammation induce recruitment of lectins in humans. METHODS: Fifteen healthy volunteers received LPS intravenously (IV) or in a lung subsegment on two different occasions. Volunteers were evaluated by consecutive blood samples and by bronchoalveolar lavage 2, 4, 6, 8, or 24h...... ficolin-3 and ficolin-1 in the lung and systemic compartment, respectively, suggesting an important role of distinct lectin complement pathway initiators in the local pulmonary and systemic host defence....

  4. Acute effect of glucan-spiked office dust on nasal and pulmonary inflammation in guinea pigs

    Straszek, Sune; Adamcakova-Dodd, Andrea; Nervana, Metwali; Pedersen, Ole Finn; Sigsgaard, Torben; Thorne, Peter Sherman

    2007-01-01

    The acute effects of pure inhaled glucan on respiratory inflammation remain inconclusive and not sufficiently examined with regards to the simultaneous interaction of glucan, endotoxin (LPS) and house dust in airway inflammation. This study aims at determining effects of simultaneous exposure to...... by acoustic rhinometry (AR) and animals were exposed by inhalation for 4 hr to curdlan spiked dust, unspiked dust, purified air (negative controls) or LPS (positive controls). After exposure (+5 hr) or the following day (+18 hr) measurements were repeated by AR and followed by bronchoalveolar lavage...... (BAL). Total and differential cell counts, IL-8 in BAL fluid and change in nasal volume was compared between groups. A 5-10% increase in nasal volume was seen for all groups including clean air except for a significant 5% decrease for spiked-dust inhalation (+18 hr). No marked differences were observed...

  5. Effect and its clinical significance of different dose of glucocorticoids on inflammation mediators in patients with acute exacerbation of chronic obstructive pulmonary diseases

    钟佰强

    2014-01-01

    Objective To explore the effect and its clinical significance of different dose of glucocorticoids on inflammation mediators in patients with acute exacerbation of chronic obstructive pulmonary diseases.Methods 45 patients admitted to our hospitals from March 2007 to March 2011were randomly divided into 3 groups:methylprednisolone40 mg group(methylprednisolone 40mg,iv,qd),meth-

  6. TRPV4 inhibition counteracts edema and inflammation and improves pulmonary function and oxygen saturation in chemically induced acute lung injury.

    Balakrishna, Shrilatha; Song, Weifeng; Achanta, Satyanarayana; Doran, Stephen F; Liu, Boyi; Kaelberer, Melanie M; Yu, Zhihong; Sui, Aiwei; Cheung, Mui; Leishman, Emma; Eidam, Hilary S; Ye, Guosen; Willette, Robert N; Thorneloe, Kevin S; Bradshaw, Heather B; Matalon, Sadis; Jordt, Sven-Eric

    2014-07-15

    The treatment of acute lung injury caused by exposure to reactive chemicals remains challenging because of the lack of mechanism-based therapeutic approaches. Recent studies have shown that transient receptor potential vanilloid 4 (TRPV4), an ion channel expressed in pulmonary tissues, is a crucial mediator of pressure-induced damage associated with ventilator-induced lung injury, heart failure, and infarction. Here, we examined the effects of two novel TRPV4 inhibitors in mice exposed to hydrochloric acid, mimicking acid exposure and acid aspiration injury, and to chlorine gas, a severe chemical threat with frequent exposures in domestic and occupational environments and in transportation accidents. Postexposure treatment with a TRPV4 inhibitor suppressed acid-induced pulmonary inflammation by diminishing neutrophils, macrophages, and associated chemokines and cytokines, while improving tissue pathology. These effects were recapitulated in TRPV4-deficient mice. TRPV4 inhibitors had similar anti-inflammatory effects in chlorine-exposed mice and inhibited vascular leakage, airway hyperreactivity, and increase in elastance, while improving blood oxygen saturation. In both models of lung injury we detected increased concentrations of N-acylamides, a class of endogenous TRP channel agonists. Taken together, we demonstrate that TRPV4 inhibitors are potent and efficacious countermeasures against severe chemical exposures, acting against exaggerated inflammatory responses, and protecting tissue barriers and cardiovascular function. PMID:24838754

  7. DNA strand breaks, acute phase response and inflammation following pulmonary exposure by instillation to the diesel exhaust particle NIST1650b in mice

    Kyjovska, Zdenka O.; Jacobsen, Nicklas R.; Saber, Anne T.;

    2015-01-01

    the alkaline comet assay as DNA strand breaks in BAL cells, lung and liver tissue. The pulmonary acute phase response was analysed by Saa3 mRNA levels by real-time quantitative polymerase chain reaction. Instillation of DEP induced a strong neutrophil influx 1 and 3 days, but not 28 days post......We investigated the inflammatory response, acute phase response and genotoxic effect of diesel exhaust particles (DEPs, NIST1650b) following a single intratracheal instillation. C57BL/6J BomTac mice received 18, 54 or 162 µg/mouse and were killed 1, 3 and 28 days post-exposure. Vehicle controls and...... inflammation but long-lasting pulmonary acute phase response as well as genotoxicity in lung tissue 28 days post-exposure. The observed long-term pulmonary genotoxicity by DEP was less than the previously observed genotoxicity for CB using identical experimental set-up....

  8. Acute pulmonary inflammation induced by exposure of the airways to staphylococcal enterotoxin type B in rats

    Staphylocococcus aureus is a gram-positive bacterium that produces several enterotoxins, which are responsible for most part of pathological conditions associated to staphylococcal infections, including lung inflammation. This study aimed to investigate the underlying inflammatory mechanisms involved in leukocyte recruitment in rats exposed to staphylococcal enterotoxin B (SEB). Rats were anesthetized with pentobarbital sodium and intratracheally injected with either SEB or sterile phosphate-buffered saline (PBS, 0.4 ml). Airways exposition to SEB (7.5-250 ng/trachea) caused a dose- and time-dependent neutrophil accumulation in BAL fluid, the maximal effects of which were observed at 4 h post-SEB exposure (250 ng/trachea). Eosinophils were virtually absent in BAL fluid, whereas mononuclear cell counts increased only at 24 h post-SEB. Significant elevations of granulocytes in bone marrow (mature and immature forms) and peripheral blood have also been detected. In BAL fluid, marked elevations in the levels of lipid mediators (LTB4 and PGE2) and cytokines (TNF-α, IL-6 and IL-10) were observed after SEB instillation. The SEB-induced neutrophil accumulation in BAL fluid was reduced by pretreatment with dexamethasone (0.5 mg/kg), the COX-2 inhibitor celecoxib (3 mg/kg), the selective iNOS inhibitor compound 1400 W (5 mg/kg) and the lipoxygenase inhibitor AA-861 (200 μg/kg). In separate experiments carried out with rat isolated peripheral neutrophils, SEB failed to induce neutrophil adhesion to serum-coated plates and chemotaxis. In conclusion, rat airways exposition to SEB causes a neutrophil-dependent lung inflammation at 4 h as result of the release of proinflammatory (NO, PGE2, LTB4, TNF-α, IL-6) and anti-inflammatory mediators (IL-10)

  9. Potentiated interaction between ineffective doses of budesonide and formoterol to control the inhaled cadmium-induced up-regulation of metalloproteinases and acute pulmonary inflammation in rats.

    Wenhui Zhang

    Full Text Available The anti-inflammatory properties of glucocorticoids are well known but their protective effects exerted with a low potency against heavy metals-induced pulmonary inflammation remain unclear. In this study, a model of acute pulmonary inflammation induced by a single inhalation of cadmium in male Sprague-Dawley rats was used to investigate whether formoterol can improve the anti-inflammatory effects of budesonide. The cadmium-related inflammatory responses, including matrix metalloproteinase-9 (MMP-9 activity, were evaluated. Compared to the values obtained in rats exposed to cadmium, pretreatment of inhaled budesonide (0.5 mg/15 ml elicited a significant decrease in total cell and neutrophil counts in bronchoalveolar lavage fluid (BALF associated with a significant reduction of MMP-9 activity which was highly correlated with the number of inflammatory cells in BALF. Additionally, cadmium-induced lung injuries characterized by inflammatory cell infiltration within alveoli and the interstitium were attenuated by the pre-treatment of budesonide. Though the low concentration of budesonide (0.25 mg/15 ml exerted a very limited inhibitory effects in the present rat model, its combination with an inefficient concentration of formoterol (0.5 mg/30 ml showed an enhanced inhibitory effect on neutrophil and total cell counts as well as on the histological lung injuries associated with a potentiation of inhibition on the MMP-9 activity. In conclusion, high concentration of budesonide alone could partially protect the lungs against cadmium exposure induced-acute neutrophilic pulmonary inflammation via the inhibition of MMP-9 activity. The combination with formoterol could enhance the protective effects of both drugs, suggesting a new therapeutic strategy for the treatment of heavy metals-induced lung diseases.

  10. Interleukin-23-Mediated Inflammation in Pseudomonas aeruginosa Pulmonary Infection

    Dubin, Patricia J.; Martz, Ashley; Eisenstatt, Jessica R.; Fox, Michael D.; Logar, Alison; Kolls, Jay K.

    2012-01-01

    Pseudomonas aeruginosa is an opportunistic pathogen that is capable of causing acute and chronic pulmonary infection in the immunocompromised host. In the case of cystic fibrosis (CF), chronic P. aeruginosa infection causes increased mortality by promoting overly exuberant airway inflammation and cumulative lung damage. Identifying the key regulators of this inflammation may lead to the development of new therapies that improve P. aeruginosa-related mortality. We report here that interleukin-...

  11. INFLAMMATION AND ACUTE PHASE RESPONSE

    Farah Aziz Khan

    2010-10-01

    Full Text Available Inflammation caused by infection takes place by the cooperative cascade of cytokines and leukocytes. Tumor necrosis factor, interlukin-1, and interlukin-6 play important roles as proinflammatory cytokines to mediate local inflammation and activate other inflammatory cells e.g. neutrophils, monocytes, and macrophages. At least 15 different low molecular weight cytokine are secreted by activated leukocytes and are responsible for triggering acute phase response in the form of fever, leukocytosis, increased secretion of adreno corticotropic hormones, and production of acute phase proteins. Acute phase proteins are produced in liver under the influence of cytokines, which through blood stream passes to the site of inflammation and kill the pathogens by opsonization and activating complement pathways. The changes in the concentrations of positive acute-phase proteins and negative acute-phase proteins are due to the changes in their production by liver. Three of the best known acute phase proteins are C-reactive protein, serum anyloid A, and haptoglobin. Some disease states are casually related to acute phase proteins. C-reactive protein mediated compliment activation has a key role in some forms of tissue alteration such as cardiac infarction. Elevated S amyloid A levels are seen in chronic arthritis and tuberculosis. Other acute phase proteins show more moderate rise, usually less than fivefold.

  12. INFLAMMATION AND ACUTE PHASE RESPONSE

    Farah Aziz Khan; Mohd Fareed Khan

    2010-01-01

    Inflammation caused by infection takes place by the cooperative cascade of cytokines and leukocytes. Tumor necrosis factor, interlukin-1, and interlukin-6 play important roles as proinflammatory cytokines to mediate local inflammation and activate other inflammatory cells e.g. neutrophils, monocytes, and macrophages. At least 15 different low molecular weight cytokine are secreted by activated leukocytes and are responsible for triggering acute phase response in the form of fever, leukocytosi...

  13. Effects of Mikania glomerata Spreng. and Mikania laevigata Schultz Bip. ex Baker (Asteraceae) extracts on pulmonary inflammation and oxidative stress caused by acute coal dust exposure

    Freitas, T.P.; Silveira, P.C.; Rocha, L.G.; Rezin, G.T.; Rocha, J.; Citadini-Zanette, V.; Romao, P.T.; Dal-Pizzol, F.; Pinho, R.A.; Andrade, V.M.; Streck, E.L. [University Extremo Catarinense, Criciuma (Brazil)

    2008-12-15

    Several studies have reported biological effects of Mikania glomerata and Mikania laevigata, used in Brazilian folk medicine for respiratory diseases. Pneumoconiosis is characterized by pulmonary inflammation caused by coal dust exposure. In this work, we evaluated the effect of pretreatment with M. glomerata and M. laevigata extracts (MGE and MLE, respectively) (100 mg/kg, s.c.) on inflammatory and oxidative stress parameters in lung of rats subjected to a single coal dust intratracheal instillation. Rats were pretreated for 2 weeks with saline solution, MGE, or MLE. On day 15, the animals were anesthetized, and gross mineral coal dust or saline solutions were administered directly in the lung by intratracheal instillation. Fifteen days after coal dust instillation, the animals were killed. Bronchoalveolar lavage (BAL) was obtained; total cell count and lactate dehydrogenase (LDH) activity were determined. In the lung, myeloperoxidase activity, thiobarbituric acid-reactive substances (TBARS) level, and protein carbonyl and sulfhydryl contents were evaluated. In BAL of treated animals, we verified an increased total cell count and LDH activity. MGE and MLE prevented the increase in cell count, but only MLE prevented the increase in LDH. Myeloperoxidase and TBARS levels were not affected, protein carbonylation was increased, and the protein thiol levels were decreased by acute coal dust intratracheal administration. The findings also suggest that both extracts present an important protective effect on the oxidation of thiol groups. Moreover, pretreatment with MGE and MLE also diminished lung inflammatory infiltration induced by coal dust, as assessed by histopathologic analyses.

  14. Ozone-Induced Pulmonary Injury and Inflammation are Modulated by Adrenal-Derived Stress Hormones

    Ozone exposure promotes pulmonary injury and inflammation. Previously we have characterized systemic changes that occur immediately after acute ozone exposure and are mediated by neuro-hormonal stress response pathway. Both HPA axis and sympathetic tone alterations induce the rel...

  15. The dynamics of acute inflammation

    Kumar, Rukmini

    The acute inflammatory response is the non-specific and immediate reaction of the body to pathogenic organisms, tissue trauma and unregulated cell growth. An imbalance in this response could lead to a condition commonly known as "shock" or "sepsis". This thesis is an attempt to elucidate the dynamics of acute inflammatory response to infection and contribute to its systemic understanding through mathematical modeling and analysis. The models of immunity discussed use Ordinary Differential Equations (ODEs) to model the variation of concentration in time of the various interacting species. Chapter 2 discusses three such models of increasing complexity. Sections 2.1 and 2.2 discuss smaller models that capture the core features of inflammation and offer general predictions concerning the design of the system. Phase-space and bifurcation analyses have been used to examine the behavior at various parameter regimes. Section 2.3 discusses a global physiological model that includes several equations modeling the concentration (or numbers) of cells, cytokines and other mediators. The conclusions drawn from the reduced and detailed models about the qualitative effects of the parameters are very similar and these similarities have also been discussed. In Chapter 3, the specific applications of the biologically detailed model are discussed in greater detail. These include a simulation of anthrax infection and an in silico simulation of a clinical trial. Such simulations are very useful to biologists and could prove to be invaluable tools in drug design. Finally, Chapter 4 discusses the general problem of extinction of populations modeled as continuous variables in ODES is discussed. The average time to extinction and threshold are estimated based on analyzing the equivalent stochastic processes.

  16. Resolution of acute inflammation in the lung.

    Levy, Bruce D; Serhan, Charles N

    2014-01-01

    Acute inflammation in the lung is essential to health. So too is its resolution. In response to invading microbes, noxious stimuli, or tissue injury, an acute inflammatory response is mounted to protect the host. To limit inflammation and prevent collateral injury of healthy, uninvolved tissue, the lung orchestrates the formation of specialized proresolving mediators, specifically lipoxins, resolvins, protectins, and maresins. These immunoresolvents are agonists for resolution that interact with specific receptors on leukocytes and structural cells to blunt further inflammation and promote catabasis. This process appears to be defective in several common lung diseases that are characterized by excess or chronic inflammation. Here, we review the molecular and cellular effectors of resolution of acute inflammation in the lung. PMID:24313723

  17. Nutrition, Inflammation, and Acute Pancreatitis

    Max Petrov

    2013-01-01

    Acute pancreatitis is acute inflammatory disease of the pancreas. Nutrition has a number of anti-inflammatory effects that could affect outcomes of patients with pancreatitis. Further, it is the most promising nonspecific treatment modality in acute pancreatitis to date. This paper summarizes the best available evidence regarding the use of nutrition with a view of optimising clinical management of patients with acute pancreatitis.

  18. Pulmonary edema in acute carbon monoxide poisoning

    Acute carbon monoxide poisoning has frequently occurred in Korean, because of the coal briquette being widely used as fuel in Korean residences. Carbon monoxide poisoning has been extensively studied, but it has been sparsely reported that pulmonary edema may develop in acute CO poisoning. We have noticed nine cases of pulmonary edema in acute CO poisoning last year. Other possible causes of pulmonary edema could be exclude in all cases but one. The purpose of this paper is to describe nine cases of pulmonary edema complicated in acute CO poisoning and discuss the pathogenesis and the prognosis

  19. New insights into pulmonary inflammation in cystic fibrosis

    Rao, S; Grigg, J

    2006-01-01

    Persistent lower airway infection with inflammation is the major cause of morbidity and mortality in cystic fibrosis. This review examines the recent advances in the understanding of airway inflammation in cystic fibrosis, and focuses on the evidence that pulmonary inflammation is, under some circumstances, disassociated from infection, and the potential implications for therapeutic intervention.

  20. Inflammation: a trigger for acute coronary syndrome.

    Sager, Hendrik B; Nahrendorf, Matthias

    2016-09-01

    Atherosclerosis is a chronic inflammatory disease of the vessel wall and a major cause of death worldwide. One of atherosclerosis' most dreadful complications are acute coronary syndromes that comprise ST-segment elevation myocardial infarction, non-ST-segment elevation myocardial infarction, and unstable angina. We now understand that inflammation substantially contributes to the initiation, progression, and destabilization of atherosclerosis. In this review, we will focus on the role of inflammatory leukocytes, which are the cellular protagonists of vascular inflammation, in triggering disease progression and, ultimately, the destabilization that causes acute coronary syndromes. PMID:27273431

  1. Acute exacerbations and pulmonary hypertension in advanced idiopathic pulmonary fibrosis.

    Judge, Eoin P

    2012-07-01

    The aim of this study was to evaluate the risk factors for and outcomes of acute exacerbations in patients with advanced idiopathic pulmonary fibrosis (IPF), and to examine the relationship between disease severity and neovascularisation in explanted IPF lung tissue. 55 IPF patients assessed for lung transplantation were divided into acute (n=27) and non-acute exacerbation (n=28) groups. Haemodynamic data was collected at baseline, at the time of acute exacerbation and at lung transplantation. Histological analysis and CD31 immunostaining to quantify microvessel density (MVD) was performed on the explanted lung tissue of 13 transplanted patients. Acute exacerbations were associated with increased mortality (p=0.0015). Pulmonary hypertension (PH) at baseline and acute exacerbations were associated with poor survival (p<0.01). PH at baseline was associated with a significant risk of acute exacerbations (HR 2.217, p=0.041). Neovascularisation (MVD) was significantly increased in areas of cellular fibrosis and significantly decreased in areas of honeycombing. There was a significant inverse correlation between mean pulmonary artery pressure and MVD in areas of honeycombing. Acute exacerbations were associated with significantly increased mortality in patients with advanced IPF. PH was associated with the subsequent development of an acute exacerbation and with poor survival. Neovascularisation was significantly decreased in areas of honeycombing, and was significantly inversely correlated with mean pulmonary arterial pressure in areas of honeycombing.

  2. Immune Inflammation and Disease Progression in Idiopathic Pulmonary Fibrosis

    Balestro, Elisabetta; Calabrese, Fiorella; Turato, Graziella; Lunardi, Francesca; Bazzan, Erica; Marulli, Giuseppe; Biondini, Davide; Rossi, Emanuela; Sanduzzi, Alessandro; Rea, Federico; Rigobello, Chiara; Gregori, Dario; Baraldo, Simonetta; Spagnolo, Paolo

    2016-01-01

    The clinical course in idiopathic pulmonary fibrosis (IPF) is highly heterogeneous, with some patients having a slow progression and others an accelerated clinical and functional decline. This study aims to clinically characterize the type of progression in IPF and to investigate the pathological basis that might account for the observed differences in disease behavior. Clinical and functional data were analyzed in 73 IPF patients, followed long-time as candidates for lung transplantation. The forced vital capacity (FVC) change/year (< or ≥10% predicted) was used to define “slow” or “rapid” disease progression. Pathological abnormalities were quantified in the explanted lung of 41 out of 73 patients undergoing lung transplantation. At diagnosis, slow progressors (n = 48) showed longer duration of symptoms and lower FVC than rapid progressors (n = 25). Eleven slow and 3 rapid progressors developed an acute exacerbation (AE) during follow-up. Quantitative lung pathology showed a severe innate and adaptive inflammatory infiltrate in rapid progressors, markedly increased compared to slow progressors and similar to that observed in patients experiencing AE. The extent of inflammation was correlated with the yearly FVC decline (r = 0.52, p = 0.005). In conclusion an innate and adaptive inflammation appears to be a prominent feature in the lung of patients with IPF and could contribute to determining of the rate of disease progression. PMID:27159038

  3. Mediators of Inflammation in Acute Kidney Injury

    Ali Akcay; Quocan Nguyen; Edelstein, Charles L.

    2010-01-01

    Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathopathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the in...

  4. Resolvins: Natural Agonists for Resolution of Pulmonary Inflammation

    Uddin, Mohib; Levy, Bruce D.

    2010-01-01

    Inappropriate or excessive pulmonary inflammation can contribute to chronic lung diseases. In health, the resolution of inflammation is an active process that terminates inflammatory responses. The recent identification of endogenous lipid-derived mediators of resolution has provided a window to explore the pathobiology of inflammatory disease and structural templates for the design of novel pro-resolving therapeutics. Resolvins (resolution-phase interaction products) are a family of pro-reso...

  5. Acute pulmonary embolism in helical computed tomography

    Pulmonary embolism is a common condition in which diagnostic and therapeutic delays contribute to substantial morbidity and mortality. Clinical diagnosis is difficult because the signs and symptoms re unspecific, and a differential diagnosis is extensive, including pneumonia or bronchitis, asthma, myocardial infraction, pulmonary edema, anxiety, dissection of the aorta, pericardial tamponade, lung cancer, primary pulmonary hypertension, rib fracture, and pneumothorax. The purpose of the study was to present the use of CT in diagnosing acute pulmonary embolism. A group of 23 patients with clinically suspected pulmonary embolism underwent CT examination with a helical CT scanner (Somatom Emotion, Siemens) before and after administration of 150 ml of Ultravist. Pulmonary embolism was found in the CT examinations of 13 patients. In two of these it was a central filling defect. Amputation of the artery was found in one. Parietal filling defect in three patients formed an acute angle with the vessel walls. Saddle emboli appearing as filling defects in the contrast column that hung over vessel bifurcations was found in two patients. In five patients,emboli were found in small segmental arteries. CT provides information not only on the pulmonary arteries, but also on the lung parenchyma, hila, mediastinum, and the heart. Alternative findings may be identified by CT chest examination, stablishing alternative diagnoses, including pulmonary disorders (such as pneumonia or fibrosis), pleural abnormalities, and cardiovascular disease (such as aortic dissection or pericardial tamponade). Another advantage of the CT is its widespread availability.(author)

  6. Acute pulmonary parenchymal densities in the adult

    The thrust of the radiographic interpretation is to correlate the often non-specific appearance of any parenchymal density with its time-table of development, rate of change, distribution, and the patient's clinical status. Although this chapter contains separate sections on each major cause of acute pulmonary opacification, the intent of the chapter overall is their differential diagnosis. Before beginning to deal with acute pulmonary densities, it is stressed that acute densities can only be differentiated from chronic ones by reviewing preoperative or pre-existing studies. Without the baseline comparison film or reliable presumption of prior normalcy, the acuteness of a parenchymal density may not be apparent until later examinations reveal change or resolution. Also, as discussed is baseline pathology that is altered by the portable technique can be terribly confusing when attempting to evaluate a single isolated film in an acute clinical situation

  7. Amiodarone-induced pulmonary toxicity mimicking acute pulmonary edema.

    Fabiani, Iacopo; Tacconi, Danilo; Grotti, Simone; Brandini, Rossella; Salvadori, Claudia; Caremani, Marcello; Bolognese, Leonardo

    2011-05-01

    Amiodarone is a highly effective antiarrhythmic drug. Its long-term use may, however, lead to several adverse effects, with pulmonary toxicity being the most serious. The article presents the case of a 78-year-old woman with a history of cardiac surgery, who after 2 years of amiodarone therapy for prophylactic treatment of atrial fibrillation developed amiodarone pneumonitis mimicking an acute pulmonary edema. The patient failed to respond to diuretic therapy and several courses of anti-infective therapy. Differential diagnosis of different causes of pulmonary infiltrates did not demonstrate any other abnormality. Lung biopsy findings were consistent with the diagnosis of amiodarone pneumonitis. Given the widespread use of amiodarone as an antiarrhythmic agent, pneumologists and cardiologists should consider this important adverse effect as a differential diagnosis of pulmonary distress refractory to therapy in all patients treated with amiodarone who present with respiratory symptoms and pneumonia-like illness. PMID:19924000

  8. Acute pulmonary embolism: the clinical conundrum

    WANG Zeng-li

    2012-01-01

    Despite important advances in the diagnosis and treatment of acute pulmonary embolism (APE),assessment of risk and appropriate management of patients remains a difficult task in clinical practice.In addition to hemodynamic instability and critically clinical condition,acute right ventricular dysfunction (RVD) is a major determinant of in-hospital outcomes.The purpose of this review is to discuss the results of these recent developments.Some outcome evaluation,clinical assessment,and therapeutic implications are also included.

  9. Aggravating Impact of Nanoparticles on Immune-Mediated Pulmonary Inflammation

    Ken-Ichiro Inoue; Hirohisa Takano

    2011-01-01

    Although the adverse health effects of nanoparticles have been proposed and are being clarified, their aggravating effects on pre-existing pathological conditions have not been fully investigated. In this review, we provide insights into the immunotoxicity of both airborne and engineered nanoparticles as an exacerbating factor on hypersusceptible subjects, especially those with immune-mediated pulmonary inflammation, using our in vivo experimental model. First, we exhibit the effects of nanop...

  10. Endothelial Semaphorin 7A Promotes Inflammation in Seawater Aspiration-Induced Acute Lung Injury

    Minlong Zhang

    2014-10-01

    Full Text Available Inflammation is involved in the pathogenesis of seawater aspiration-induced acute lung injury (ALI. Although several studies have shown that Semaphorin 7A (SEMA7A promotes inflammation, there are limited reports regarding immunological function of SEMA7A in seawater aspiration-induced ALI. Therefore, we investigated the role of SEMA7A during seawater aspiration-induced ALI. Male Sprague–Dawley rats were underwent seawater instillation. Then, lung samples were collected at an indicated time for analysis. In addition, rat pulmonary microvascular endothelial cells (RPMVECs were cultured and then stimulated with 25% seawater for indicated time point. After these treatments, cells samples were collected for analysis. In vivo, seawater instillation induced lung histopathologic changes, pro-inflammation cytokines release and increased expression of SEMA7A. In vitro, seawater stimulation led to pro-inflammation cytokine release, cytoskeleton remodeling and increased monolayer permeability in pulmonary microvascular endothelial cells. In addition, knockdown of hypoxia-inducible factor (HIF-1α inhibited the seawater induced increase expression of SEMA7A. Meanwhile, knockdown of SEMA7A by specific siRNA inhibited the seawater induced aberrant inflammation, endothelial cytoskeleton remodeling and endothelial permeability. These results suggest that SEMA7A is critical in the development of lung inflammation and pulmonary edema in seawater aspiration-induced ALI, and may be a therapeutic target for this disease.

  11. Pulmonary CD103 expression regulates airway inflammation in asthma.

    Bernatchez, Emilie; Gold, Matthew J; Langlois, Anick; Lemay, Anne-Marie; Brassard, Julyanne; Flamand, Nicolas; Marsolais, David; McNagny, Kelly M; Blanchet, Marie-Renee

    2015-04-15

    Although CD103(+) cells recently emerged as key regulatory cells in the gut, the role of CD103 ubiquitous expression in the lung and development of allergic airway disease has never been studied. To answer this important question, we evaluated the response of Cd103(-/-) mice in two separate well-described mouse models of asthma (ovalbumin and house dust mite extract). Pulmonary inflammation was assessed by analysis of bronchoalveolar lavage content, histology, and cytokine response. CD103 expression was analyzed on lung dendritic cells and T cell subsets by flow cytometry. Cd103(-/-) mice exposed to antigens developed exacerbated lung inflammation, characterized by increased eosinophilic infiltration, severe tissue inflammation, and altered cytokine response. In wild-type mice exposed to house dust mite, CD103(+) dendritic cells are increased in the lung and an important subset of CD4(+) T cells, CD8(+) T cells, and T regulatory cells express CD103. Importantly, Cd103(-/-) mice presented a deficiency in the resolution phase of inflammation, which supports an important role for this molecule in the control of inflammation severity. These results suggest an important role for CD103 in the control of airway inflammation in asthma. PMID:25681437

  12. Inhibition of chlorine-induced pulmonary inflammation and edema by mometasone and budesonide

    Chen, Jing; Mo, Yiqun; Schlueter, Connie F.; Hoyle, Gary W., E-mail: Gary.Hoyle@louisville.edu

    2013-10-15

    Chlorine gas is a widely used industrial compound that is highly toxic by inhalation and is considered a chemical threat agent. Inhalation of high levels of chlorine results in acute lung injury characterized by pneumonitis, pulmonary edema, and decrements in lung function. Because inflammatory processes can promote damage in the injured lung, anti-inflammatory therapy may be of potential benefit for treating chemical-induced acute lung injury. We previously developed a chlorine inhalation model in which mice develop epithelial injury, neutrophilic inflammation, pulmonary edema, and impaired pulmonary function. This model was used to evaluate nine corticosteroids for the ability to inhibit chlorine-induced neutrophilic inflammation. Two of the most potent corticosteroids in this assay, mometasone and budesonide, were investigated further. Mometasone or budesonide administered intraperitoneally 1 h after chlorine inhalation caused a dose-dependent inhibition of neutrophil influx in lung tissue sections and in the number of neutrophils in lung lavage fluid. Budesonide, but not mometasone, reduced the levels of the neutrophil attractant CXCL1 in lavage fluid 6 h after exposure. Mometasone or budesonide also significantly inhibited pulmonary edema assessed 1 day after chlorine exposure. Chlorine inhalation resulted in airway hyperreactivity to inhaled methacholine, but neither mometasone nor budesonide significantly affected this parameter. The results suggest that mometasone and budesonide may represent potential treatments for chemical-induced lung injury. - Highlights: • Chlorine causes lung injury when inhaled and is considered a chemical threat agent. • Corticosteroids may inhibit lung injury through their anti-inflammatory actions. • Corticosteroids inhibited chlorine-induced pneumonitis and pulmonary edema. • Mometasone and budesonide are potential rescue treatments for chlorine lung injury.

  13. Impact of interleukin-6 on hypoxia-induced pulmonary hypertension and lung inflammation in mice

    Izziki Mohamed

    2009-01-01

    Full Text Available Abstract Background Inflammation may contribute to the pathogenesis of various forms of pulmonary hypertension (PH. Recent studies in patients with idiopathic PH or PH associated with underlying diseases suggest a role for interleukin-6 (IL-6. Methods To determine whether endogenous IL-6 contributes to mediate hypoxic PH and lung inflammation, we studied IL-6-deficient (IL-6-/- and wild-type (IL-6+/+ mice exposed to hypoxia for 2 weeks. Results Right ventricular systolic pressure, right ventricle hypertrophy, and the number and media thickness of muscular pulmonary vessels were decreased in IL-6-/- mice compared to wild-type controls after 2 weeks' hypoxia, although the pressure response to acute hypoxia was similar in IL-6+/+ and IL-6-/- mice. Hypoxia exposure of IL-6+/+ mice led to marked increases in IL-6 mRNA and protein levels within the first week, with positive IL-6 immunostaining in the pulmonary vessel walls. Lung IL-6 receptor and gp 130 (the IL-6 signal transducer mRNA levels increased after 1 and 2 weeks' hypoxia. In vitro studies of cultured human pulmonary-artery smooth-muscle-cells (PA-SMCs and microvascular endothelial cells revealed prominent synthesis of IL-6 by PA-SMCs, with further stimulation by hypoxia. IL-6 also markedly stimulated PA-SMC migration without affecting proliferation. Hypoxic IL-6-/- mice showed less inflammatory cell recruitment in the lungs, compared to hypoxic wild-type mice, as assessed by lung protein levels and immunostaining for the specific macrophage marker F4/80, with no difference in lung expression of adhesion molecules or cytokines. Conclusion These data suggest that IL-6 may be actively involved in hypoxia-induced lung inflammation and pulmonary vascular remodeling in mice.

  14. Rosette nanotubes show low acute pulmonary toxicity in vivo

    W Shane Journeay

    2008-10-01

    Full Text Available W Shane Journeay1, Sarabjeet S Suri1, Jesus G Moralez2, Hicham Fenniri2, Baljit Singh11Immunology Research Group, Toxicology Graduate Program and Department of Veterinary Biomedical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, SK, S7N 5B4, Canada; 2National Institute of Nanotechnology, National Research Council (NINT-NRC and Department of Chemistry, University of Alberta, 11421 Saskatchewan Drive, Edmonton, AB, T6G 2M9, CanadaAbstract: Nanotubes are being developed for a large variety of applications ranging from electronics to drug delivery. Common carbon nanotubes such as single-walled and multi-walled carbon nanotubes have been studied in the greatest detail but require solubilization and removal of catalytic contaminants such as metals prior to being introduced to biological systems for medical application. The present in vivo study characterizes the degree and nature of inflammation caused by a novel class of self-assembling rosette nanotubes, which are biologically inspired, naturally water-soluble and free of metal content upon synthesis. Upon pulmonary administration of this material we examined responses at 24 h and 7d post-exposure. An acute inflammatory response is triggered at 50 and 25 μg doses by 24 h post-exposure but an inflammatory response is not triggered by a 5 μg dose. Lung inflammation observed at a 50 μg dose at 24 h was resolving by 7d. This work suggests that novel nanostructures with biological design may negate toxicity concerns for biomedical applications of nanotubes. This study also demonstrates that water-soluble rosette nanotube structures represent low pulmonary toxicity, likely due to their biologically inspired design, and their self-assembled architecture.Keywords: nanotoxicology, biocompatibility, nanomedicine, pulmonary drug delivery, lung inflammation

  15. Pulmonary Artery Denervation Reduces Pulmonary Artery Pressure and Induces Histological Changes in an Acute Porcine Model of Pulmonary Hypertension

    Rothman, A.M.K.; Arnold, N D; Chang, W.; Watson, O.; Swift, A J; Condliffe, R; Elliot, C A; Kiely, D. G.; Suvarna, S K; Gunn, J.; Lawrie, A.

    2015-01-01

    Background— Pulmonary arterial hypertension is a devastating disease with high morbidity and mortality and limited treatment options. Recent studies have shown that pulmonary artery denervation improves pulmonary hemodynamics in an experimental model and in an early clinical trial. We aimed to evaluate the nerve distribution around the pulmonary artery, to determine the effect of radiofrequency pulmonary artery denervation on acute pulmonary hypertension induced by vasoconstriction, and to de...

  16. Impaired respiratory function and heightened pulmonary inflammation in episodic binge ethanol intoxication and burn injury.

    Shults, Jill A; Curtis, Brenda J; Chen, Michael M; O'Halloran, Eileen B; Ramirez, Luis; Kovacs, Elizabeth J

    2015-11-01

    Clinical data indicate that cutaneous burn injuries covering greater than 10% of the total body surface area are associated with significant morbidity and mortality, in which pulmonary complications, including acute respiratory distress syndrome (ARDS), contribute to nearly half of all patient deaths. Approximately 50% of burn patients are intoxicated at the time of hospital admission, which increases days on ventilators by 3-fold, and doubles the length of hospitalization, compared to non-intoxicated burn patients. The most common drinking pattern in the United States is binge drinking, where an individual rapidly consumes alcoholic beverages (4 for women, 5 for men) in 2 h. An estimated 38 million Americans binge drink, often several times per month. Experimental data demonstrate that a single binge-ethanol exposure, prior to scald injury, impairs innate and adaptive immune responses, thereby enhancing infection susceptibility and amplifying pulmonary inflammation, neutrophil infiltration, and edema, and is associated with increased mortality. Since these characteristics are similar to those observed in ARDS burn patients, our study objective was to determine whether ethanol intoxication and burn injury and the subsequent pulmonary congestion affect physiological parameters of lung function, using non-invasive and unrestrained plethysmography in a murine model system. Furthermore, to mirror young adult binge-drinking patterns, and to determine the effect of multiple ethanol exposures on pulmonary inflammation, we utilized an episodic binge-ethanol exposure regimen, where mice were exposed to ethanol for a total of 6 days (3 days ethanol, 4 days rest, 3 days ethanol) prior to burn injury. Our analyses demonstrate mice exposed to episodic binge ethanol and burn injury have higher mortality, increased pulmonary congestion and neutrophil infiltration, elevated neutrophil chemoattractants, and respiratory dysfunction, compared to burn or ethanol intoxication alone

  17. Chronic Thromboembolic Pulmonary Hypertension Associated with Chronic Inflammation.

    Kuse, Naoyuki; Abe, Shinji; Kuribayashi, Hidehiko; Fukuda, Asami; Kusunoki, Yuji; Narato, Ritsuko; Saito, Hitoshi; Gemma, Akihiko

    2016-01-01

    Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the leading causes of severe pulmonary hypertension. According to previously reported studies in the pertinent literature, chronic inflammatory conditions may be implicated in the development of CTEPH. We herein describe the case of a 56-year-old woman who was diagnosed with CTEPH in association with chronic infection. The patient had experienced five episodes of pneumonia in the five years prior to the diagnosis of CTEPH. Blood tests from the previous five years of outpatient follow-up demonstrated that the C-reactive protein level was slightly elevated. This case suggests that a relationship exists between chronic inflammation and CTEPH, and furthermore, may contribute towards elucidating the pathophysiology of CTEPH. PMID:27250055

  18. Acute pulmonary rejection in heart and lung transplant recipients

    Acute pulmonary rejection occurs in up to 50% of patients undergoing heart and lung transplant procedures. These patients are also susceptible to volume overload and pneumonia. To evaluate the radiographic and high-resolution CT appearances of acute pulmonary rejection, we compared chest radiographs and high-resolution CT scans with the clinical findings and with histologic and lavage data from 91 serial transbronchial biopsies in 13 patients. The radiographic appearance of acute pulmonary rejection is characterized by prominent septal lines and pleural effusions. The authors conclude that in the appropriate clinical setting, the appearance of new pleural effusions and prominent septal lines is highly suggestive of acute pulmonary rejections

  19. Negative spiral CT in acute pulmonary embolism

    Purpose: To retrospectively evaluate the clinical outcome of non-anticoagulated patients with clinically suspected acute pulmonary embolism (PE) and no symptoms or signs of deep venous thrombosis (DVT) following a negative contrast medium-enhanced spiral CT of the pulmonary arteries (s-CTPA). Material and Methods: During a 24-month period, 739 of 751 patients underwent s-CTPA with acceptable diagnostic quality for clinically suspected acute PE. All patients who had a CT study not positive for PE were followed up with a questionnaire, a telephone interview and review of all medical reports, including autopsies and death certificates for any episodes of venous thromboembolism (VTE) during a 3-month period. Results: PE was diagnosed in 158 patients. Of the remaining 581 patients with a negative s-CTPA, 45 patients were lost to follow-up. 88 patients were excluded because of anticoagulation treatment (cardiac disorder n=32, chronic VTE or acute symptomatic DVT n=31, PE diagnosed at pulmonary angiography n=1, thrombus prophylaxis during diagnostic work-up or other reasons than VTE n=24) and 7 patients undergoing lower extremity venous studies because of symptoms of DVT (all negative). Thus, 441 patients with a negative s-CTPA and no DVT symptoms, venous studies or anticoagulant treatment constituted the follow-up cohort. Four of these patients had proven VTE (all PE) during the 3-month follow-up period. Two of the PE episodes contributed to the patient's death. Conclusion: Patients with clinically suspected acute PE, no symptoms or signs of DVT and a negative single slice s-CTPA using 3-5 mm collimation, may safely be left without anticoagulation treatment unless they are critically ill, have a limited cardiopulmonary reserve and/or if a high clinical suspicion remains

  20. Comparative imaging study in experimental acute pulmonary embolism

    Objective: To evaluate the diagnostic characteristics of radionuclide pulmonary perfusion imaging, enhanced spiral computed tomography, and digital subtraction pulmonary angiography in acute experimental segmental pulmonary embolism (corresponding to human subsegmental pulmonary embolism). Methods: Acute pulmonary embolism model was established in thirteen Chinese small type pigs by injecting glutin embolus (the diameter of the embolus was 3.8 to 4.2 mm) into pulmonary artery via jugular vein, and then radionuclide pulmonary perfusion imaging, enhanced spiral computed tomography and digital subtraction pulmonary angiography were performed. The results of sensitivity and specificity of three kinds of imaging methods were compared with the pathological findings. Results: Out of 195 segmental pulmonary arteries, abnormalities were found in forty-six segmental pulmonary arteries by pathological study. Abnormalities were detected in fifty-one segmental pulmonary arteries by pulmonary perfusion imaging, with sensitivity of 87%, specificity 93%. Filling defect was demonstrated in forty-four segmental pulmonary arteries by enhanced spiral computed tomography, with sensitivity of 63%, specificity 89%. Abnormalities were displayed in forty-seven segmental pulmonary arteries by digital subtraction pulmonary angiography, with sensitivity of 98%, specificity 99%. Pulmonary perfusion imaging was superior to enhanced spiral computed tomography (P0.05). Conclusions: Pulmonary perfusion imaging is a noninvasive technique for diagnosis of pulmonary embolism which is superior to enhanced spiral computed tomography in detecting of experimental acute segmental pulmonary embolism (corresponding to human subsegmental pulmonary embolism), but the localization of embolus is more accurate by enhanced spiral computed tomography. Combination of three kinds of imaging methods may significantly improve the diagnostic accuracy for pulmonary embolism

  1. Lung inflammation does not affect the clearance kinetics of lipid nanocapsules following pulmonary administration.

    Patel, Aateka; Woods, A; Riffo-Vasquez, Yanira; Babin-Morgan, Anna; Jones, Marie-Christine; Jones, Stuart; Sunassee, Kavitha; Clark, Stephen; T M de Rosales, Rafael; Page, Clive; Spina, Domenico; Forbes, Ben; Dailey, Lea Ann

    2016-08-10

    Lipid nanocapsules (LNCs) are semi-rigid spherical capsules with a triglyceride core that present a promising formulation option for the pulmonary delivery of drugs with poor aqueous solubility. Whilst the biodistribution of LNCs of different size has been studied following intravenous administration, the fate of LNCs following pulmonary delivery has not been reported. We investigated quantitatively whether lung inflammation affects the clearance of 50nm lipid nanocapsules, or is exacerbated by their pulmonary administration. Studies were conducted in mice with lipopolysaccharide-induced lung inflammation compared to healthy controls. Particle deposition and nanocapsule clearance kinetics were measured by single photon emission computed tomography/computed tomography (SPECT/CT) imaging over 48 h. A significantly lower lung dose of (111)In-LNC50 was achieved in the lipopolysaccharide (LPS)-treated animals compared with healthy controls (p<0.001). When normalised to the delivered lung dose, the clearance kinetics of (111)In-LNC50 from the lungs fit a first order model with an elimination half-life of 10.5±0.9h (R(2)=0.995) and 10.6±0.3h (R(2)=1.000) for healthy and inflamed lungs respectively (n=3). In contrast, (111)In-diethylene triamine pentaacetic acid (DTPA), a small hydrophilic molecule, was cleared rapidly from the lungs with the majority of the dose absorbed within 20min of administration. Biodistribution to lungs, stomach-intestine, liver, trachea-throat and blood at the end of the imaging period was unaltered by lung inflammation. This study demonstrated that lung clearance and whole body distribution of lipid nanocapsules were unaffected by the presence of acute lung inflammation. PMID:27180635

  2. IKK NBD peptide inhibits LPS induced pulmonary inflammation and alters sphingolipid metabolism in a murine model.

    von Bismarck, Philipp; Winoto-Morbach, Supandi; Herzberg, Mona; Uhlig, Ulrike; Schütze, Stefan; Lucius, Ralph; Krause, Martin F

    2012-06-01

    Airway epithelial NF-κB is a key regulator of host defence in bacterial infections and has recently evolved as a target for therapeutical approaches. Evidence is accumulating that ceramide, generated by acid sphingomyelinase (aSMase), and sphingosine-1-phosphate (S1-P) are important mediators in host defence as well as in pathologic processes of acute lung injury. Little is known about the regulatory mechanisms of pulmonary sphingolipid metabolism in bacterial infections of the lung. The objective of this study was to evaluate the influence of NF-κB on sphingolipid metabolism in Pseudomonas aeruginosa LPS-induced pulmonary inflammation. In a murine acute lung injury model with intranasal Pseudomonas aeruginosa LPS we investigated TNF-α, KC (murine IL-8), IL-6, MCP-1 and neutrophilic infiltration next to aSMase activity and ceramide and S1-P lung tissue concentrations. Airway epithelial NF-κB was inhibited by topically applied IKK NBD, a cell penetrating NEMO binding peptide. This treatment resulted in significantly reduced inflammation and suppression of aSMase activity along with decreased ceramide and S1-P tissue concentrations down to levels observed in healthy animals. In conclusion our results confirm that changes in sphingolipid metabolim due to Pseudomonas aeruginosa LPS inhalation are regulated by NF-κB translocation. This confirms the critical role of airway epithelial NF-κB pathway for the inflammatory response to bacterial pathogens and underlines the impact of sphingolipids in inflammatory host defence mechanisms. PMID:22469869

  3. The X-ray analysis of pulmonary manifestations in acute aspiration of trichlorethane

    Objective: To discuss the X-ray pulmonary changes in patients with acute aspiration of trichlorethane. Methods: Among 48 cases with acute aspiration of trichlorethane, 7 were male and 41 female, with ages ranged from 5.5 to 50 years old, mean age was 13.5 years old. 4 patients were diagnosed as mild acute intoxication, 22 as aspirating reaction, and 22 as uncomfortable reaction. And chest radiography was performed in all the cases. Results Pneumonia and bronchopneumonia was found in 4 cases with acute intoxication, inflammation around bronchial branches in 22 cases with aspirating reaction. The other cases were negative findings. Conclusions: Acute aspiration of trichlorethane may cause pneumonia, bronchopneumonia and inflammation around bronchial branches, which can be detected by chest radiography. (authors)

  4. Anti-inflammatory effects of naringin in chronic pulmonary neutrophilic inflammation in cigarette smoke-exposed rats

    Nie, YC; Wu, H.; Li, PB; Luo, YL; Long, K.; Xie, LM; Shen, JG; Su, WW

    2012-01-01

    Naringin, a well-known flavanone glycoside of grapefruit and citrus fruits, was found to be as an effective anti-inflammatory compound in our previous lipopolysaccharide-induced acute lung injury mouse model via blockading activity of nuclear factor κB. The current study sought to explore the anti-inflammatory effects of naringin on chronic pulmonary neutrophilic inflammation in cigarette smoke (CS)-induced rats. Seventy Sprague-Dawley rats were randomly divided into seven groups to study the...

  5. Multidetector computed tomography pulmonary angiography in childhood acute pulmonary embolism

    Pulmonary embolism is a life-threatening condition affecting people of all ages. Multidetector row CT pulmonary angiography has improved the imaging of pulmonary embolism in both adults and children and is now regarded as the routine modality for detection of pulmonary embolism. Advanced CT pulmonary angiography techniques developed in recent years, such as dual-energy CT, have been applied as a one-stop modality for pulmonary embolism diagnosis in children, as they can simultaneously provide anatomical and functional information. We discuss CT pulmonary angiography techniques, common and uncommon findings of pulmonary embolism in both conventional and dual-energy CT pulmonary angiography, and radiation dose considerations. (orig.)

  6. Multidetector computed tomography pulmonary angiography in childhood acute pulmonary embolism

    Tang, Chun Xiang; Zhang, Long Jiang; Lu, Guang Ming [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Schoepf, U.J. [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States); Medical University of South Carolina, Department of Pediatrics, Charleston, SC (United States); Chowdhury, Shahryar M. [Medical University of South Carolina, Department of Pediatrics, Charleston, SC (United States); Fox, Mary A. [Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States)

    2015-09-15

    Pulmonary embolism is a life-threatening condition affecting people of all ages. Multidetector row CT pulmonary angiography has improved the imaging of pulmonary embolism in both adults and children and is now regarded as the routine modality for detection of pulmonary embolism. Advanced CT pulmonary angiography techniques developed in recent years, such as dual-energy CT, have been applied as a one-stop modality for pulmonary embolism diagnosis in children, as they can simultaneously provide anatomical and functional information. We discuss CT pulmonary angiography techniques, common and uncommon findings of pulmonary embolism in both conventional and dual-energy CT pulmonary angiography, and radiation dose considerations. (orig.)

  7. Inflammation and airway microbiota during cystic fibrosis pulmonary exacerbations.

    Edith T Zemanick

    Full Text Available BACKGROUND: Pulmonary exacerbations (PEx, frequently associated with airway infection and inflammation, are the leading cause of morbidity in cystic fibrosis (CF. Molecular microbiologic approaches detect complex microbiota from CF airway samples taken during PEx. The relationship between airway microbiota, inflammation, and lung function during CF PEx is not well understood. OBJECTIVE: To determine the relationships between airway microbiota, inflammation, and lung function in CF subjects treated for PEx. METHODS: Expectorated sputum and blood were collected and lung function testing performed in CF subjects during early (0-3d. and late treatment (>7d. for PEx. Sputum was analyzed by culture, pyrosequencing of 16S rRNA amplicons, and quantitative PCR for total and specific bacteria. Sputum IL-8 and neutrophil elastase (NE; and circulating C-reactive protein (CRP were measured. RESULTS: Thirty-seven sputum samples were collected from 21 CF subjects. At early treatment, lower diversity was associated with high relative abundance (RA of Pseudomonas (r = -0.67, p<0.001, decreased FEV(1% predicted (r = 0.49, p = 0.03 and increased CRP (r = -0.58, p = 0.01. In contrast to Pseudomonas, obligate and facultative anaerobic genera were associated with less inflammation and higher FEV₁. With treatment, Pseudomonas RA and P. aeruginosa by qPCR decreased while anaerobic genera showed marked variability in response. Change in RA of Prevotella was associated with more variability in FEV₁ response to treatment than Pseudomonas or Staphylococcus. CONCLUSIONS: Anaerobes identified from sputum by sequencing are associated with less inflammation and higher lung function compared to Pseudomonas at early exacerbation. CF PEx treatment results in variable changes of anaerobic genera suggesting the need for larger studies particularly of patients without traditional CF pathogens.

  8. Thioredoxin-1 protects against neutrophilic inflammation and emphysema progression in a mouse model of chronic obstructive pulmonary disease exacerbation.

    Naoya Tanabe

    Full Text Available BACKGROUND: Exacerbations of chronic obstructive pulmonary disease (COPD are characterized by acute enhancement of airway neutrophilic inflammation under oxidative stress and can be involved in emphysema progression. However, pharmacotherapy against the neutrophilic inflammation and emphysema progression associated with exacerbation has not been established. Thioredoxin-1 has anti-oxidative and anti-inflammatory properties and it can ameliorate neutrophilic inflammation through anti-chemotactic effects and prevent cigarette smoke (CS-induced emphysema. We aimed to determine whether thioredoxin-1 can suppress neutrophilic inflammation and emphysema progression in a mouse model of COPD exacerbation and if so, to reveal the underlying mechanisms. RESULTS: Mice were exposed to CS and then challenged with polyinosine-polycytidylic acid [poly(I:C], an agonist for virus-induced innate immunity. Airway neutrophilic inflammation, oxidative stress and lung apoptosis were enhanced in smoke-sensitive C57Bl/6, but not in smoke-resistant NZW mice. Exposure to CS and poly(I:C challenge accelerated emphysema progression in C57Bl/6 mice. Thioredoxin-1 suppressed neutrophilic inflammation and emphysema progression. Poly(I:C caused early neutrophilic inflammation through keratinocyte-derived chemokine and granulocyte-macrophage colony-stimulating factor (GM-CSF release in the lung exposed to CS. Late neutrophilic inflammation was caused by persistent GM-CSF release, which thioredoxin-1 ameliorated. Thioredoxin-1 enhanced pulmonary mRNA expression of MAP kinase phosphatase 1 (MKP-1, and the suppressive effects of thioredoxin-1 on prolonged GM-CSF release and late neutrophilic inflammation disappeared by inhibiting MKP-1. CONCLUSION: Using a mouse model of COPD exacerbation, we demonstrated that thioredoxin-1 ameliorated neutrophilic inflammation by suppressing GM-CSF release, which prevented emphysema progression. Our findings deepen understanding of the mechanisms

  9. Present state of radiological diagnostics in acute pulmonary failure

    Acute pulmonary failure is a very serious cause of respiratory failure. Radiological diagnosis occupies a central position in intensive-care monitoring. X-ray film of the thorax is performed not only for detecting any complications, but mainly for noninvasive and semiquantitative determination of the extravascular pulmonary fluid and hence of the fluid balance. Other methods such as MR or methods of nuclear medicine have not acquired substantial importance in respect of diagnosis and monitoring acute pulmonary failure. (orig./GDG)

  10. Silver Nanoparticles: A study of dissolution, kinetics, and factors affecting pulmonary inflammation

    Saunders, Eric L.

    The growing use of silver (Ag) nanoparticles (NP) in consumer and industrial goods has led to an increase in interest in the health effects associated with exposure, both occupationally and environmentally. The aim of this research is to examine the contribution of size, shape, and dissolution of AgNP, with its corresponding effect on pulmonary inflammation and clearance. In addition this study looks at metallothionein (MT) and the role it plays as an inflammatory modulator. A nose only exposure method was used to expose three strains of mouse (two inbred, one knockout) to two different sizes of AgNP (˜25 nm and ˜100 nm). This research demonstrates that size, chemistry, and dissolution play key roles in NP deposition and inflammatory response, while no conclusions could be drawn about shape. Additionally, this study found that the main factors affecting the deposition of NP in mice both acutely and sub-chronically are particle size and mouse strain. The results of this study also indicate a relationship between MT2 and inflammation. It was found that the mRNA levels of MT2 were greatly up-regulated in the livers and lungs of mice exposed to AgNP, while MT protein levels were not significantly altered to correlate with the altered regulation of mRNA. Finally, this study showed that, for AgNP, the mechanisms of pulmonary clearance and dissolution happened rapidly and that they, combined, likely represent a major pathway of AgNP transport out of the lung. Taken as a whole, the data in this study show that dissolution, coupled with protein interaction, is a significant mediator of pulmonary inflammation and translocation of AgNP.

  11. Inactivation of capsaicin-sensitive nerves reduces pulmonary remodeling in guinea pigs with chronic allergic pulmonary inflammation

    C.M. Prado; G.Z. da Rocha; E.A. Leick-Maldonado; C.M. Starling; V.L. Capelozzi; M. A. Martins; I.F.L.C. Tibério

    2011-01-01

    Pulmonary remodeling is an important feature of asthma physiopathology that can contribute to irreversible changes in lung function. Although neurokinins influence lung inflammation, their exact role in the extracellular matrix (ECM) remodeling remains to be determined. Our objective was to investigate whether inactivation of capsaicin-sensitive nerves modulates pulmonary ECM remodeling in animals with chronic lung inflammation. After 14 days of capsaicin (50 mg/kg, sc) or vehicle administrat...

  12. Grouping nanomaterials to predict their potential to induce pulmonary inflammation.

    Braakhuis, Hedwig M; Oomen, Agnes G; Cassee, Flemming R

    2016-05-15

    The rapidly expanding manufacturing, production and use of nanomaterials have raised concerns for both worker and consumer safety. Various studies have been published in which induction of pulmonary inflammation after inhalation exposure to nanomaterials has been described. Nanomaterials can vary in aspects such as size, shape, charge, crystallinity, chemical composition, and dissolution rate. Currently, efforts are made to increase the knowledge on the characteristics of nanomaterials that can be used to categorise them into hazard groups according to these characteristics. Grouping helps to gather information on nanomaterials in an efficient way with the aim to aid risk assessment. Here, we discuss different ways of grouping nanomaterials for their risk assessment after inhalation. Since the relation between single intrinsic particle characteristics and the severity of pulmonary inflammation is unknown, grouping of nanomaterials by their intrinsic characteristics alone is not sufficient to predict their risk after inhalation. The biokinetics of nanomaterials should be taken into account as that affects the dose present at a target site over time. The parameters determining the kinetic behaviour are not the same as the hazard-determining parameters. Furthermore, characteristics of nanomaterials change in the life-cycle, resulting in human exposure to different forms and doses of these nanomaterials. As information on the biokinetics and in situ characteristics of nanomaterials is essential but often lacking, efforts should be made to include these in testing strategies. Grouping nanomaterials will probably be of the most value to risk assessors when information on intrinsic characteristics, life-cycle, biokinetics and effects are all combined. PMID:26603513

  13. Particle-induced pulmonary acute phase response may be the causal link between particle inhalation and cardiovascular disease

    Saber, Anne T.; Jacobsen, Nicklas R.; Jackson, Petra;

    2014-01-01

    Inhalation of ambient and workplace particulate air pollution is associated with increased risk of cardiovascular disease. One proposed mechanism for this association is that pulmonary inflammation induces a hepatic acute phase response, which increases risk of cardiovascular disease. Induction of...... epidemiological studies. In this review, we present and review emerging evidence that inhalation of particles (e.g., air diesel exhaust particles and nanoparticles) induces a pulmonary acute phase response, and propose that this induction constitutes the causal link between particle inhalation and risk of...... cardiovascular disease. Increased levels of acute phase mRNA and proteins in lung tissues, bronchoalveolar lavage fluid and plasma clearly indicate pulmonary acute phase response following pulmonary deposition of different kinds of particles including diesel exhaust particles, nanoparticles, and carbon nanotubes...

  14. Pulmonary vascular-bronchial interactions: acute reduction in pulmonary blood flow alters lung mechanics

    Schulze-Neick, I; Penny, D; Derrick, G; Dhillon, R; Rigby, M.; Kelleher, A.; Bush, A; Redington, A

    2000-01-01

    BACKGROUND—Postoperative pulmonary hypertension in children after congenital heart surgery is a risk factor for death and is associated with severe acute changes in both pulmonary vascular resistance and lung mechanics.
OBJECTIVE—To examine the impact of changes in pulmonary blood flow on lung mechanics in preoperative children with congenital heart disease, in order to assess the cause-effect relation of pulmonary vascular-bronchial interactions.
DESIGN—Prospective, cross sectional study.
SE...

  15. Acute chlorine gas exposure produces transient inflammation and a progressive alteration in surfactant composition with accompanying mechanical dysfunction

    Acute Cl2 exposure following industrial accidents or military/terrorist activity causes pulmonary injury and severe acute respiratory distress. Prior studies suggest that antioxidant depletion is important in producing dysfunction, however a pathophysiologic mechanism has not been elucidated. We propose that acute Cl2 inhalation leads to oxidative modification of lung lining fluid, producing surfactant inactivation, inflammation and mechanical respiratory dysfunction at the organ level. C57BL/6J mice underwent whole-body exposure to an effective 60 ppm-hour Cl2 dose, and were euthanized 3, 24 and 48 h later. Whereas pulmonary architecture and endothelial barrier function were preserved, transient neutrophilia, peaking at 24 h, was noted. Increased expression of ARG1, CCL2, RETLNA, IL-1b, and PTGS2 genes was observed in bronchoalveolar lavage (BAL) cells with peak change in all genes at 24 h. Cl2 exposure had no effect on NOS2 mRNA or iNOS protein expression, nor on BAL NO3− or NO2−. Expression of the alternative macrophage activation markers, Relm-α and mannose receptor was increased in alveolar macrophages and pulmonary epithelium. Capillary surfactometry demonstrated impaired surfactant function, and altered BAL phospholipid and surfactant protein content following exposure. Organ level respiratory function was assessed by forced oscillation technique at 5 end expiratory pressures. Cl2 exposure had no significant effect on either airway or tissue resistance. Pulmonary elastance was elevated with time following exposure and demonstrated PEEP refractory derecruitment at 48 h, despite waning inflammation. These data support a role for surfactant inactivation as a physiologic mechanism underlying respiratory dysfunction following Cl2 inhalation. - Highlights: • Effect of 60 ppm*hr Cl2 gas on lung inflammation and mechanical function examined. • Pulmonary inflammation is transient and minor. • Alterations in surfactant homeostasis and pulmonary mechanics

  16. Coincident helminth infection modulates systemic inflammation and immune activation in active pulmonary tuberculosis.

    Parakkal Jovvian George

    Full Text Available Helminth infections are known to modulate innate and adaptive immune responses in active and latent tuberculosis (TB. However, the role of helminth infections in modulating responses associated with inflammation and immune activation (reflecting disease activity and/or severity in TB is not known.We measured markers of inflammation and immune activation in active pulmonary TB individuals (ATB with co-incidental Strongyloides stercoralis (Ss infection. These included systemic levels of acute phase proteins, matrix metalloproteinases and their endogenous inhibitors and immune activation markers. As a control, we measured the systemic levels of the same molecules in TB-uninfected individuals (NTB with or without Ss infection.Our data confirm that ATB is associated with elevated levels of the various measured molecules when compared to those seen in NTB. Our data also reveal that co-incident Ss infection in ATB individuals is associated with significantly decreased circulating levels of acute phase proteins, matrix metalloproteinases, tissue inhibitors of matrix metalloproteinases as well as the systemic immune activation markers, sCD14 and sCD163. These changes are specific to ATB since they are absent in NTB individuals with Ss infection.Our data therefore reveal a profound effect of Ss infection on the markers associated with TB disease activity and severity and indicate that co-incidental helminth infections might dampen the severity of TB disease.

  17. Spred-2 deficiency exacerbates lipopolysaccharide-induced acute lung inflammation in mice.

    Yang Xu

    Full Text Available BACKGROUND: Acute respiratory distress syndrome (ARDS is a severe and life-threatening acute lung injury (ALI that is caused by noxious stimuli and pathogens. ALI is characterized by marked acute inflammation with elevated alveolar cytokine levels. Mitogen-activated protein kinase (MAPK pathways are involved in cytokine production, but the mechanisms that regulate these pathways remain poorly characterized. Here, we focused on the role of Sprouty-related EVH1-domain-containing protein (Spred-2, a negative regulator of the Ras-Raf-extracellular signal-regulated kinase (ERK-MAPK pathway, in lipopolysaccharide (LPS-induced acute lung inflammation. METHODS: Wild-type (WT mice and Spred-2(-/- mice were exposed to intratracheal LPS (50 µg in 50 µL PBS to induce pulmonary inflammation. After LPS-injection, the lungs were harvested to assess leukocyte infiltration, cytokine and chemokine production, ERK-MAPK activation and immunopathology. For ex vivo experiments, alveolar macrophages were harvested from untreated WT and Spred-2(-/- mice and stimulated with LPS. In in vitro experiments, specific knock down of Spred-2 by siRNA or overexpression of Spred-2 by transfection with a plasmid encoding the Spred-2 sense sequence was introduced into murine RAW264.7 macrophage cells or MLE-12 lung epithelial cells. RESULTS: LPS-induced acute lung inflammation was significantly exacerbated in Spred-2(-/- mice compared with WT mice, as indicated by the numbers of infiltrating leukocytes, levels of alveolar TNF-α, CXCL2 and CCL2 in a later phase, and lung pathology. U0126, a selective MEK/ERK inhibitor, reduced the augmented LPS-induced inflammation in Spred-2(-/- mice. Specific knock down of Spred-2 augmented LPS-induced cytokine and chemokine responses in RAW264.7 cells and MLE-12 cells, whereas Spred-2 overexpression decreased this response in RAW264.7 cells. CONCLUSIONS: The ERK-MAPK pathway is involved in LPS-induced acute lung inflammation. Spred-2 controls

  18. Familial idiopathic pulmonary fibrosis. Evidence of lung inflammation in unaffected family members

    We evaluated 17 clinically unaffected members of three families with an autosomal dominant form of idiopathic pulmonary fibrosis for evidence of alveolar inflammation. Each person in the study was examined by gallium-67 scanning for a general estimate of pulmonary inflammation, and by bronchoalveolar lavage for characterization of the types of recovered cells and their state of activation. Eight of the 17 subjects had evidence of alveolar inflammation on the lavage studies. Supporting data included increased numbers of neutrophils and activated macrophages that released one or more neutrophil chemoattractants, and growth factors for lung fibroblasts--findings similar to those observed in patients with overt idiopathic pulmonary fibrosis. Four of these eight also had a positive gallium scan; in all the other clinically unaffected subjects the scan was normal. During a follow-up of two to four years in seven of the eight subjects who had evidence of inflammation, no clinical evidence of pulmonary fibrosis has appeared. These results indicate that alveolar inflammation occurs in approximately half the clinically unaffected family members at risk of inheriting autosomal dominant idiopathic pulmonary fibrosis. Whether these persons with evidence of pulmonary inflammation but no fibrosis will proceed to have clinically evident pulmonary fibrosis is not yet known

  19. Acute Toxic Myocarditis and Pulmonary Oedema Developing from Scorpion Sting

    Cem Sahin; Ethem Acar; Halil Beydilli; Kadir Ugur Mert; Fatih Akin; Ibrahim Altun

    2015-01-01

    The majority of scorpion stings are generally seen with a set of simple clinical findings, such as pain, oedema, numbness, and tenderness in the area of the sting. However, occasionally events, such as toxic myocarditis, acute heart failure, acute pulmonary oedema, and Acute Respiratory Distress Syndrome (ARDS), which occur in scorpion sting cases are a significant problem which determine mortality and morbidity. The case presented here was a 38-year-old man who developed acute toxic myocardi...

  20. Acute Sin Nombre hantavirus infection without pulmonary syndrome, United States.

    Kitsutani, P. T.; Denton, R. W.; Fritz, C. L.; Murray, R. A.; Todd, R. L.; Pape, W. J.; Wyatt Frampton, J.; Young, J C; Khan, A. S.; Peters, C. J.; Ksiazek, T. G.

    1999-01-01

    Hantavirus pulmonary syndrome (HPS) occurs in most infections with Sin Nombre virus and other North American hantaviruses. We report five cases of acute hantavirus infection that did not fit the HPS case definition. The patients had characteristic prodromal symptoms without severe pulmonary involvement. These cases suggest that surveillance for HPS may need to be expanded.

  1. Protease Activation and Inflammation in Acute Pancreatitis

    Regnér, Sara

    2008-01-01

    Approximately 10—20 % of patients with acute pancreatitis (AP) develop a severe disease with high mortality and morbidity. Activation of pancreatic proteases, the inflammatory response and impaired pancreatic circulation are pathophysiological events that are important in order for the disease to develop. There is no specific treatment for severe AP, and no useful marker for predicting the severity of the disease upon admission to the hospital. In this thesis, markers of early pathophysio...

  2. Acute respiratory distress syndrome: Pulmonary and extrapulmonary not so similar

    Inderpaul Singh Sehgal; Sahajal Dhooria; Digambar Behera; Ritesh Agarwal

    2016-01-01

    Acute respiratory distress syndrome (ARDS) is characterized by acute onset respiratory failure with bilateral pulmonary infiltrates and hypoxemia. Current evidence suggests different respiratory mechanics in pulmonary ARDS (ARDSp) and extrapulmonary ARDS (ARDSexp) with disproportionate decrease in lung compliance in the former and chest wall compliance in the latter. Herein, we report two patients of ARDS, one each with ARDSp and ARDSexp that were managed using real-time esophageal pressure m...

  3. Protective role of interleukin-10 in Ozone-induced pulmonary inflammation**

    Background: The mechanisms underlying ozone (03)-induced pulmonary inflammation remain unclear. Interleukin-10 (IL-10) is an anti-inflammatory cytokine that is known to inhibit inflammatory mediators. Objectives: We investigated the molecular mechanisms underlying interleuken-10...

  4. Pulmonary oxidative stress, inflammation and dysregulated iron homeostatis in rat models of cardiovascular disease

    Underlying cardiovascular disease (CVD) is considered a risk factor for the exacerbation of air pollution health effects. Therefore, rodent models of CVD are increasingly used to examine mechanisms ofvariation in susceptibility. Pulmonary oxidative stress, inflammation and altere...

  5. Evolution of pulmonary inflammation and nutritional status in infants and young children with cystic fibrosis

    Ranganathan, Sarath C; Parsons, Faith; Gangell, Catherine; Brennan, Siobhan; Stick, Stephen M.; Peter D Sly

    2011-01-01

    Introduction Improved nutrition is the major proven benefit of newborn screening programmes for cystic fibrosis (CF) and is associated with better clinical outcomes. It was hypothesised that early pulmonary inflammation and infection in infants with CF is associated with worse nutrition. Methods Weight, height and pulmonary inflammation and infection in bronchoalveolar lavage (BAL) were assessed shortly after diagnosis in infants with CF and again at 1, 2 and 3 year...

  6. Acute pulmonary embolism following air travel

    Ledermann, J. A.; Keshavarzian, Ali

    1983-01-01

    Three cases of pulmonary embolism following long air flight are described. There was no previous history of venous disease. The symptoms were transient in one and severe in two. The occurrence of pulmonary embolism immediately after air travel is emphasized.

  7. Intratracheal administration of endotoxin and cytokines. IV. The soluble tumor necrosis factor receptor type I inhibits acute inflammation.

    Ulich, T R; Yin, S.; Remick, D G; Russell, D; Eisenberg, S P; Kohno, T

    1993-01-01

    Endotoxin lipopolysaccharide (LPS) administered intratracheally to rats causes pulmonary tumor necrosis factor alpha (TNF) and interleukin-1 (IL-1) production and results in acute broncho-alveolar neutrophilic inflammation. In the present study, the recombinant human TNF soluble receptor type I (sTNFrI) co-injected intratracheally with LPS is shown to inhibit significantly (P < 0.0001) the number of neutrophils in bronchoalveolar lavage specimens at 6 hours as compared to intratracheal inject...

  8. Digital subtraction angiography (DSA) for acute pulmonary emboli

    The results of 49 DSAs (in 29 patients) are presented; these were performed for the diagnosis or follow-up of pulmonary emboli. The direct or indirect signs of pulmonary emboli, known to occur during conventional pulmonary angiography, were used as diagnostic criteria. In 47 examinations it was possible to make or to exclude the diagnosis unequivocally. The advantages of DSA make it desirable to use this method as the first form of examination in the diagnosis of acute, but not immediately life-threatening, pulmonary emboli. (orig.)

  9. CT and pathologic correlation acute miliary pulmonary tuberculosis

    Objective: To elucidate the CT characteristics and pathology of acute miliary pulmonary tuberculosis (AMPT). Methods: The CT features of AMPT in 25 cases were analyzed retrospectively, and the CT features in HIV-seronegative and HIV-seropositive patients were compared by 2-sided exact probability Chi-square test. Two lung specimens were inflated and fixed by Heitzman's method. HRCT scans, gross specimen section (80-150 μm) and histologic section (5 μm) were performed on dry lung specimens and CT-pathologic correlation was conducted. The distribution of micronodules in the secondary lobule on HRCT and pathology in one specimen was evaluated by Chi-square test. Results: Twenty five patients with AMPT were included in this study, including 11 HIV-seropositive patients and 14 HIV- seronegative patients. HRCT showed diffuse micronodules randomly distributed throughout both lungs in 25 patients, and ground-glass opacity (17 patients) was the predominant complicated finding. Coalescence of nodules and consolidation in HIV-seropositive patients (5 and 6 patients) were markedly higher than that in HIV-seronegative patients (none). In lung specimens, most nodules located in the lung parenchyma between the central bronchovascular bundle and the perilobular structures (792 and 560 nodules), which located in the interlobular septum pathologically. The distribution of micronodules in the secondary lobule showed on HRCT (1060 nodules) and pathology (864 nodules) was not significantly difference (χ2=2.814, P>0.05) . HRCT showed ground-glass opacities when ARDS occurred, which were pulmonary edema, inflammation and hyaline membrane on alveolar wall pathologically. Conclusions: The HRCT characteristic of nodule distribution in AMPT is random. ARDS should be suspected when diffuse ground-glass opacities appear on HRCT. (authors)

  10. Pulmonary thromboembolic disease. Clinical management of acute and chronic disease.

    Torbicki, Adam

    2010-07-01

    Pulmonary thromboembolism falls between the areas of pulmonology and cardiology, internal medicine and intensive care, radiology and nuclear medicine, and hematology and cardiothoracic surgery. Depending on their clinical background, physicians faced with a patient with a pulmonary thromboembolism may speak different languages and adopt different treatment approaches. Now, however, there is an opportunity to end the Tower of Babel surrounding pulmonary thromboembolism. There is a growing acknowledgement that the key clinical problems in both acute pulmonary embolism and chronic thromboembolic pulmonary hypertension are linked to right ventricular pressure overload and right ventricular failure. As a result, cardiologists and cardiac intensive care specialists are taking an increasing interest in understanding and combating these conditions. The European Society of Cardiology was the first to elaborate comprehensive clinical practice guidelines for pulmonary thromboembolism and chronic thromboembolic pulmonary hypertension. The task forces involved in producing these guidelines included radiologists, pulmonologists, hematologists, intensive care physicians and surgeons, which ensured that the final document was universally acceptable. The aim of this article was to provide an overview of the epidemiology, risk factors, diagnosis, treatment, prognosis and prevention of acute pulmonary thromboembolism and chronic thromboembolic pulmonary hypertension, while taking into account European Society of Cardiology guidelines and incorporating new evidence where necessary. PMID:20609317

  11. Creatine kinase activity in dogs with experimentally induced acute inflammation

    Dimitrinka Zapryanova

    2013-01-01

    Full Text Available The main purpose of this study was to investigate the effect of acute inflammation on total creatine kinase (CK activity in dogs. In these animals, CK is an enzyme found predominantly in skeletal muscle and significantly elevated serum activity is largely associated with muscle damage. Plasma increases in dogs are associated with cell membrane leakage and will therefore be seen in any condition associated with muscular inflammation. The study was induced in 15 mongrel male dogs (n=9 in experimental group and n=6 in control group at the age of two years and body weight 12-15 kg. The inflammation was reproduced by inoculation of 2 ml turpentine oil subcutaneously in lumbar region. The plasma activity of creatine kinase was evaluated at 0, 6, 24, 48, 72 hours after inoculation and on days 7, 14 and 21 by a kit from Hospitex Diagnostics. In the experimental group, the plasma concentrations of the CK-activity were increased at the 48th hour (97.48±6.92 U/L and remained significantly higher (p<0.05 at the 72 hour (97.43±2.93 U/L compared to the control group (77.08±5.27 U/L. The results of this study suggest that the evaluation of creatine kinase in dogs with experimentally induced acute inflammation has a limited diagnostic value. It was observed that the creatine kinase activity is slightly affected by the experimentally induced acute inflammation in dogs.

  12. CT pulmonary angiography findings that predict 30-day mortality in patients with acute pulmonary embolism

    Bach, Andreas Gunter, E-mail: mail@andreas-bach.de [Department of Radiology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Germany); Nansalmaa, Baasai; Kranz, Johanna [Department of Radiology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Germany); Taute, Bettina-Maria [Department of Internal Medicine, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Germany); Wienke, Andreas [Institute of Medical Epidemiology, Biostatistics and Informatics, Martin-Luther-University Halle-Wittenberg, Magdeburger-Str. 8, 06112 Halle (Germany); Schramm, Dominik; Surov, Alexey [Department of Radiology, Martin-Luther-University Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Germany)

    2015-02-15

    Highlights: • In patients with acute pulmonary embolism contrast reflux in inferior vena cava is significantly stronger in non-survivors (odds ratio 3.29; p < 0.001). • This finding is independent from the following comorbidities: heart insufficiency and pulmonary hypertension. • Measurement of contrast reflux is a new and robust radiologic method for predicting 30-day mortality in patients with acute pulmonary embolism. • Measurement of contrast reflux is a better predictor of 30-day mortality after acute pulmonary embolism than any other existing radiologic predictor. This includes thrombus distribution, and morphometric measurements of right ventricular dysfunction. - Abstract: Purpose: Standard computed tomography pulmonary angiography (CTPA) can be used to diagnose acute pulmonary embolism. In addition, multiple findings at CTPA have been proposed as potential tools for risk stratification. Therefore, the aim of the present study is to examine the prognostic value of (I) thrombus distribution, (II) morphometric parameters of right ventricular dysfunction, and (III) contrast reflux in inferior vena cava on 30-day mortality. Material and methods: In a retrospective, single-center study from 06/2005 to 01/2010 365 consecutive patients were included. Inclusion criteria were: presence of acute pulmonary embolism, and availability of 30-day follow-up. A review of patient charts and images was performed. Results: There were no significant differences between the group of 326 survivors and 39 non-survivors in (I) thrombus distribution, and (II) morphometric measurements of right ventricular dysfunction. However, (III) contrast reflux in inferior vena cava was significantly stronger in non-survivors (odds ratio 3.29; p < 0.001). Results were independent from comorbidities like heart insufficiency and pulmonary hypertension. Conclusion: Measurement of contrast reflux is a new and robust method for predicting 30-day mortality in patients with acute pulmonary

  13. CT pulmonary angiography findings that predict 30-day mortality in patients with acute pulmonary embolism

    Highlights: • In patients with acute pulmonary embolism contrast reflux in inferior vena cava is significantly stronger in non-survivors (odds ratio 3.29; p < 0.001). • This finding is independent from the following comorbidities: heart insufficiency and pulmonary hypertension. • Measurement of contrast reflux is a new and robust radiologic method for predicting 30-day mortality in patients with acute pulmonary embolism. • Measurement of contrast reflux is a better predictor of 30-day mortality after acute pulmonary embolism than any other existing radiologic predictor. This includes thrombus distribution, and morphometric measurements of right ventricular dysfunction. - Abstract: Purpose: Standard computed tomography pulmonary angiography (CTPA) can be used to diagnose acute pulmonary embolism. In addition, multiple findings at CTPA have been proposed as potential tools for risk stratification. Therefore, the aim of the present study is to examine the prognostic value of (I) thrombus distribution, (II) morphometric parameters of right ventricular dysfunction, and (III) contrast reflux in inferior vena cava on 30-day mortality. Material and methods: In a retrospective, single-center study from 06/2005 to 01/2010 365 consecutive patients were included. Inclusion criteria were: presence of acute pulmonary embolism, and availability of 30-day follow-up. A review of patient charts and images was performed. Results: There were no significant differences between the group of 326 survivors and 39 non-survivors in (I) thrombus distribution, and (II) morphometric measurements of right ventricular dysfunction. However, (III) contrast reflux in inferior vena cava was significantly stronger in non-survivors (odds ratio 3.29; p < 0.001). Results were independent from comorbidities like heart insufficiency and pulmonary hypertension. Conclusion: Measurement of contrast reflux is a new and robust method for predicting 30-day mortality in patients with acute pulmonary

  14. Epigenetic coordination of acute systemic inflammation: potential therapeutic targets

    Vachharajani, Vidula; Liu, Tiefu; McCall, Charles E.

    2014-01-01

    Epigenetic reprogramming of thousands of genes directs the course of acute systemic inflammation, which is highly lethal when dysregulated during sepsis. No molecular-based treatments for sepsis are available. A new concept supports that sepsis is an immunometabolic disease and that loss of control of nuclear epigenetic regulator Sirtuin 1 (SIRT-1), a NAD+ sensor directs immune and metabolic pathways during sepsis. SIRT-1, acting as homeostasis checkpoint, controls hyper and hypo inflammatory...

  15. Pathophysiology of pulmonary hypertension in acute lung injury

    Price, Laura C.; Mcauley, Danny F.; Marino, Philip S; Finney, Simon J; Griffiths, Mark J.; Wort, Stephen John

    2012-01-01

    Acute lung injury (ALI) and acute respiratory distress syndrome are characterized by protein rich alveolar edema, reduced lung compliance, and acute severe hypoxemia. A degree of pulmonary hypertension (PH) is also characteristic, higher levels of which are associated with increased morbidity and mortality. The increase in right ventricular (RV) afterload causes RV dysfunction and failure in some patients, with associated adverse effects on oxygen delivery. Although the introduction of lung p...

  16. Pulmonary hypertension due to acute respiratory distress syndrome

    S.A. Ñamendys-Silva

    2014-10-01

    Full Text Available Our aims were to describe the prevalence of pulmonary hypertension in patients with acute respiratory distress syndrome (ARDS, to characterize their hemodynamic cardiopulmonary profiles, and to correlate these parameters with outcome. All consecutive patients over 16 years of age who were in the intensive care unit with a diagnosis of ARDS and an in situ pulmonary artery catheter for hemodynamic monitoring were studied. Pulmonary hypertension was diagnosed when the mean pulmonary artery pressure was >25 mmHg at rest with a pulmonary artery occlusion pressure or left atrial pressure <15 mmHg. During the study period, 30 of 402 critically ill patients (7.46% who were admitted to the ICU fulfilled the criteria for ARDS. Of the 30 patients with ARDS, 14 met the criteria for pulmonary hypertension, a prevalence of 46.6% (95% CI; 28-66%. The most common cause of ARDS was pneumonia (56.3%. The overall mortality was 36.6% and was similar in patients with and without pulmonary hypertension. Differences in patients' hemodynamic profiles were influenced by the presence of pulmonary hypertension. The levels of positive end-expiratory pressure and peak pressure were higher in patients with pulmonary hypertension, and the PaCO2 was higher in those who died. The level of airway pressure seemed to influence the onset of pulmonary hypertension. Survival was determined by the severity of organ failure at admission to the intensive care unit.

  17. PET imaging of acute and chronic inflammation in living mice

    In this study, we evaluated the 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced acute and chronic inflammation in living mice by PET imaging of TNF-α and integrin αvβ3 expression. TPA was topically applied to the right ear of BALB/c mice every other day to create the inflammation model. 64Cu-DOTA-etanercept and 64Cu-DOTA-E{E[c(RGDyK)]2}2 were used for PET imaging of TNF-α and integrin αvβ3 expression in both acute and chronic inflammation. Hematoxylin and eosin staining, ex vivo autoradiography, direct tissue sampling, and immunofluorescence staining were also performed to confirm the non-invasive PET imaging results. The ear thickness increased significantly and the TNF-α level more than tripled after a single TPA challenge. MicroPET imaging using 64Cu-DOTA-etanercept revealed high activity accumulation in the inflamed ear, reaching 11.1 ± 1.3, 13.0 ± 2.0, 10.9 ± 1.4, 10.2 ± 2.2%ID/g at 1, 4, 16, and 24 h post injection, respectively (n = 3). Repeated TPA challenges caused TPA-specific chronic inflammation and reduced 64Cu-DOTA-etanercept uptake due to lowered TNF-α expression. 64Cu-DOTA-E{E[c(RGDyK)]2}2 uptake in the chronically inflamed ears (after four and eight TPA challenges) was significantly higher than in the control ears and those after one TPA challenge. Immunofluorescence staining revealed increased integrin β3 expression, consistent with the non-invasive PET imaging results using 64Cu-DOTA-E{E[c(RGDyK)]2}2 as an integrin αv β3-specific radiotracer. Biodistribution and autoradiography studies further confirmed the quantification capability of microPET imaging. Successful PET imaging of TNF- α expression in acute inflammation and integrin αv β3 expression in chronic inflammation provides the rationale for multiple target evaluation over time to fully understand the inflammation processes. (orig.)

  18. PET imaging of acute and chronic inflammation in living mice

    Cao, Qizhen; Cai, Weibo; Li, Zi-Bo; Chen, Kai; He, Lina; Chen, Xiaoyuan [Stanford University School of Medicine, The Molecular Imaging Program at Stanford (MIPS), Department of Radiology and Bio-X Program, Stanford, CA (United States); Li, Hui-Cheng; Hui, Mizhou [AmProtein Corporation, Camarillo, CA (United States)

    2007-11-15

    In this study, we evaluated the 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced acute and chronic inflammation in living mice by PET imaging of TNF-{alpha} and integrin {alpha}{sub v}{beta}{sub 3} expression. TPA was topically applied to the right ear of BALB/c mice every other day to create the inflammation model. {sup 64}Cu-DOTA-etanercept and {sup 64}Cu-DOTA-E{l_brace}E[c(RGDyK)]{sub 2}{r_brace}{sub 2} were used for PET imaging of TNF-{alpha} and integrin {alpha}{sub v}{beta}{sub 3} expression in both acute and chronic inflammation. Hematoxylin and eosin staining, ex vivo autoradiography, direct tissue sampling, and immunofluorescence staining were also performed to confirm the non-invasive PET imaging results. The ear thickness increased significantly and the TNF-{alpha} level more than tripled after a single TPA challenge. MicroPET imaging using {sup 64}Cu-DOTA-etanercept revealed high activity accumulation in the inflamed ear, reaching 11.1 {+-} 1.3, 13.0 {+-} 2.0, 10.9 {+-} 1.4, 10.2 {+-} 2.2%ID/g at 1, 4, 16, and 24 h post injection, respectively (n = 3). Repeated TPA challenges caused TPA-specific chronic inflammation and reduced {sup 64}Cu-DOTA-etanercept uptake due to lowered TNF-{alpha} expression. {sup 64}Cu-DOTA-E{l_brace}E[c(RGDyK)]{sub 2}{r_brace}{sub 2} uptake in the chronically inflamed ears (after four and eight TPA challenges) was significantly higher than in the control ears and those after one TPA challenge. Immunofluorescence staining revealed increased integrin {beta}{sub 3} expression, consistent with the non-invasive PET imaging results using {sup 64}Cu-DOTA-E{l_brace}E[c(RGDyK)]{sub 2}{r_brace}{sub 2} as an integrin {alpha}{sub v} {beta}{sub 3}-specific radiotracer. Biodistribution and autoradiography studies further confirmed the quantification capability of microPET imaging. Successful PET imaging of TNF- {alpha} expression in acute inflammation and integrin {alpha}{sub v} {beta}{sub 3} expression in chronic inflammation provides

  19. Establishment of selected acute pulmonary thromboembolism model in experimental sheep

    Objective: To establish a selected acute pulmonary thromboembolism model in experimental sheep suitable for animal experiment. Methods: By using Seldinger's technique the catheter sheath was placed in both the femoral vein and femoral artery in ten sheep. Under C-arm DSA guidance the catheter was inserted through the catheter sheath into the pulmonary artery. Via the catheter appropriate amount of sheep autologous blood clots was injected into the selected pulmonary arteries. The selected acute pulmonary thromboembolism model was thus established. Pulmonary angiography was performed to check the results. The pulmonary arterial pressure, femoral artery pressure,heart rates and partial pressure of oxygen in arterial blood (PaO2) were determined both before and after the treatment. The above parameters obtained after the procedure were compared with the recorded parameters measured before the procedure, and the sheep model quality was evaluated. Results: The baseline of pulmonary arterial pressure was (27.30 ± 9.58) mmHg,femoral artery pressure was (126.4 ± 13.72) mmHg, heart rate was (103 ± 15) bpm and PaO2 was (87.7 ± 12.04) mmHg. Sixty minutes after the injection of (30 ± 5) ml thrombotic agglomerates, the pulmonary arterial pressures rose to (52 ± 49) mmHg, femoral artery pressures dropped to (100 ± 21) mmHg. The heart rates went up to (150 ± 26) bpm. The PaO2 fell to (25.3 ± 11.2) mmHg. After the procedure the above parameters were significantly different from that measured before the procedure in all ten animals (P < 0.01). The pulmonary arteriography clearly demonstrated that the selected pulmonary arteries were successfully embolized. Conclusion: The anatomy of sheep's femoral veins,vena cava system, pulmonary artery and right heart system are suitable for the establishment of the catheter passage, for this reason, selected acute pulmonary thromboembolism model can be easily created in experimental sheep. The technique is feasible and the model has

  20. Acute Pulmonary Response in Landscape Workers: Job Redesign

    Sexton, Pauline Lethea

    2003-01-01

    Substantial efforts have been made in the study of occupational induced airway diseases. A strong link has been found between worker exposure to organic dust and resulting acute pulmonary spasms. The supporting studies behind this link are primarily in the industries of cotton, animal and swine farming; however, some studies have been related to landscaping type tasks (i.e. mowing, leaf blowing). The relationship between organic dust and pulmonary response is associated with respiratory ir...

  1. Exposure to nickel oxide nanoparticles induces pulmonary inflammation through NLRP3 inflammasome activation in rats.

    Cao, Zhengwang; Fang, Yiliang; Lu, Yonghui; Qian, Fenghua; Ma, Qinglong; He, Mingdi; Pi, Huifeng; Yu, Zhengping; Zhou, Zhou

    2016-01-01

    With recent advances in the manufacture and application of nickel oxide nanoparticles (NiONPs), concerns about their adverse effects on the respiratory system are increasing. However, the underlying cellular and molecular mechanisms of NiONP-induced pulmonary toxicity remain unclear. In this study, we focused on the impacts of NiONPs on pulmonary inflammation and investigated whether the NLRP3 inflammasome is involved in NiONP-induced pulmonary inflammation and injury. NiONP suspensions were administered by single intratracheal instillation to rats, and inflammatory responses were evaluated at 3 days, 7 days, or 28 days after treatment. NiONP exposure resulted in sustained pulmonary inflammation accompanied by inflammatory cell infiltration, alveolar proteinosis, and cytokine secretion. Expression of Nlrp3 was markedly upregulated by the NiONPs, which was accompanied by overexpression of the active form of caspase-1 (p20) and interleukin (IL)-1β secretion in vivo. NiONP-induced IL-1β secretion was partially prevented by co-treatment with a caspase-1 inhibitor in macrophages. Moreover, siRNA-mediated Nlrp3 knockdown completely attenuated NiONP-induced cytokine release and caspase-1 activity in macrophages in vitro. In addition, NiONP-induced NLRP3 inflammasome activation requires particle uptake and reactive oxygen species production. Collectively, our findings suggest that the NLRP3 inflammasome participates in NiONP-induced pulmonary inflammation and offer new strategies to combat the pulmonary toxicity induced by NiONPs. PMID:27524893

  2. The Role of Ischemia Modified Albumin in Acute Pulmonary Embolism

    Zeynettin Kaya; M Kayrak; Gul, E. E.; G Altunbas; A Toker; Kiyici, A; M. Gunduz; Alibaşiç, H.; H Akilli; A Aribas

    2014-01-01

    Background: Acute pulmonary embolism (PE) is a life-threatening and a relatively common cardiovascular pathology. Although the pathogenesis of PE is well defined, there is no ideal diagnostic biochemical marker. Previous studies showed an increased ischemia modified albumin (IMA) levels in acute PE; however, the relationship between IMA and right ventricular (RV) dysfunction has not been examined. The aim of this study was to evaluate the diagnostic value of IMA and the relationship with RV d...

  3. Bacterial etiology in acute hospitalized chronic obstructive pulmonary disease exacerbations

    Asli Gorek Dilektasli; Ezgi Demirdogen Cetinoglu; Nilufer Aylin Acet Ozturk; Funda Coskun; Guven Ozkaya; Ahmet Ursavas; Cuneyt Ozakin; Mehmet Karadag; Esra Uzaslan

    2016-01-01

    Introduction. The most common cause of acute COPD exacerbation (AECOPD) is the respiratory tract infections. We sought to determine the bacteriological etiology of hospitalized acute exacerbations of COPD requiring hospitalization in consecutive two years. Methods. We aimed to determine the bacteriological etiology underlying in patients whom admitted to Uludag University Faculty of Medicine, Department of Pulmonary Medicine and hospitalized with AECOPD in the last two years. Medical records ...

  4. Effect of Naturally Occurring Ozone Air Pollution Episodes on Pulmonary Oxidative Stress and Inflammation

    Cheryl Pirozzi; Anne Sturrock; Hsin-Yi Weng; Tom Greene; Mary Beth Scholand; Richard Kanner; Robert Paine III

    2015-01-01

    This study aimed to determine if naturally occurring episodes of ozone air pollution in the Salt Lake Valley in Utah, USA, during the summer are associated with increased pulmonary inflammation and oxidative stress, increased respiratory symptoms, and decreased lung function in individuals with chronic obstructive pulmonary disease (COPD) compared to controls. We measured biomarkers (nitrite/nitrate (NOx), 8-isoprostane) in exhaled breath condensate (EBC), spirometry, and respiratory symptoms...

  5. The diagnostic value of pulmonary ventilation-perfusion imaging in the diagnosis of acute pulmonary thromboembolism

    Objective: The radionuclide pulmonary ventilation-perfusion (V/Q) imaging was proven useful in the diagnosis of acute pulmonary thromboembolism (PTE). The aim of the current study was to use V/Q imaging to assess the impaired states of the lung blood flow and the distributive characteristics of the damaged lung segments and lung lobes in PTE. Methods: All 519 patients with acute PTE were included in the current multi-center randomized study, with 249 massive and sub-massive PTE and 270 non-massive PTE. All 519 patients underwent pulmonary V/Q imaging. Of 519 patients with pulmonary V/Q imaging, 773 scans were compared with the findings of spiral CT pulmonary arteriography (CTPA). Results: Before treatment, the total detection rates of PTE with pulmonary V/Q imaging and CTPA were 93.3% and 89.3% (P>0.05), the detection rates of massive and sub-massive PTE were 86.9% and 100% (P<0.01); and the detection rates of non-massive PTE were 98.2% and 77.5% respectively (P <0.001). In pulmonary V/Q imaging, the defects in the right lung, lower lobe and superior segment were more likely affected than that in the left. Conclusion: Radionuclide pulmonary V/Q imaging plays an important and special role in the diagnosis of acute PTE. The combination of pulmonary V/Q imaging and CTPA can be a crucial diagnostic approach. The thrombotic distribution in the lung of PTE patients is in accordant with 'concentration conservation law. (authors)

  6. 255 Chronic Obstructive Pulmonary Disease and Lung Cancer Share Inflammation Pathways

    Kostas N. Syrigos; POLITI, EKATERINI; Makrilia, Nektaria; Tsimpoukis, Sotirios; Psarros, Fotis; Syrigou, Ekaterini; Dannos, Ioannis

    2012-01-01

    Background The relationship between inflammation, air obstruction and lung cancer is complex and there is still great uncertainty regarding their underlying pathophysiology. Our aim was to investigate the inflammation pathways that are implicated in both chronic obstructive pulmonary disease (COPD) and lung cancer. Methods A literature search was performed in PubMed to identify relative studies published until June 2011. Results The pathophysiology of both COPD and lung cancer includes dysreg...

  7. Eosinophilic airway inflammation: role in asthma and chronic obstructive pulmonary disease

    George, Leena; Brightling, Christopher E.

    2016-01-01

    The chronic lung diseases, asthma and chronic obstructive pulmonary disease (COPD), are common affecting over 500 million people worldwide and causing substantial morbidity and mortality. Asthma is typically associated with Th2-mediated eosinophilic airway inflammation, in contrast to neutrophilic inflammation observed commonly in COPD. However, there is increasing evidence that the eosinophil might play an important role in 10–40% of patients with COPD. Consistently in both asthma and COPD a...

  8. Acute pulmonary embolism. Part 1: epidemiology and diagnosis

    R.A. Douma; P.W. Kamphuisen; H.R. Büller

    2010-01-01

    Pulmonary embolism (PE) is a frequently occurring, acute, and potentially fatal condition. Numerous risk factors for PE, both inherited and acquired, have been identified. Adequate diagnosis is mandatory to prevent PE-related morbidity and mortality on the one hand, and unnecessary treatment on the

  9. Acute pulmonary embolism. Part 1: Epidemiology and diagnosis

    Douma, Renée A.; Kamphuisen, Pieter W.; Büller, Harry R.

    2010-01-01

    Pulmonary embolism (PE) is a frequently occurring, acute, and potentially fatal condition. Numerous risk factors for PE, both inherited and acquired, have been identified. Adequate diagnosis is mandatory to prevent PE-related morbidity and mortality on the one hand, and unnecessary treatment on the

  10. Pathophysiology of acute mountain sickness and high altitude pulmonary oedema

    Sutton, J R; Lassen, N

    1979-01-01

    We review the evidence that acute mountain sickness (AMS) and high altitude pulmonary oedema (HAPO) occur together more often than is realized. We hypothesize that AMS and HAPO have a common pathophysiological basis: both are due to increased pressure and flow in the microcirculation, causing...

  11. Acute chlorine gas exposure produces transient inflammation and a progressive alteration in surfactant composition with accompanying mechanical dysfunction

    Massa, Christopher B.; Scott, Pamela; Abramova, Elena; Gardner, Carol; Laskin, Debra L.; Gow, Andrew J., E-mail: Gow@rci.rutgers.edu

    2014-07-01

    Acute Cl{sub 2} exposure following industrial accidents or military/terrorist activity causes pulmonary injury and severe acute respiratory distress. Prior studies suggest that antioxidant depletion is important in producing dysfunction, however a pathophysiologic mechanism has not been elucidated. We propose that acute Cl{sub 2} inhalation leads to oxidative modification of lung lining fluid, producing surfactant inactivation, inflammation and mechanical respiratory dysfunction at the organ level. C57BL/6J mice underwent whole-body exposure to an effective 60 ppm-hour Cl{sub 2} dose, and were euthanized 3, 24 and 48 h later. Whereas pulmonary architecture and endothelial barrier function were preserved, transient neutrophilia, peaking at 24 h, was noted. Increased expression of ARG1, CCL2, RETLNA, IL-1b, and PTGS2 genes was observed in bronchoalveolar lavage (BAL) cells with peak change in all genes at 24 h. Cl{sub 2} exposure had no effect on NOS2 mRNA or iNOS protein expression, nor on BAL NO{sub 3}{sup −} or NO{sub 2}{sup −}. Expression of the alternative macrophage activation markers, Relm-α and mannose receptor was increased in alveolar macrophages and pulmonary epithelium. Capillary surfactometry demonstrated impaired surfactant function, and altered BAL phospholipid and surfactant protein content following exposure. Organ level respiratory function was assessed by forced oscillation technique at 5 end expiratory pressures. Cl{sub 2} exposure had no significant effect on either airway or tissue resistance. Pulmonary elastance was elevated with time following exposure and demonstrated PEEP refractory derecruitment at 48 h, despite waning inflammation. These data support a role for surfactant inactivation as a physiologic mechanism underlying respiratory dysfunction following Cl{sub 2} inhalation. - Highlights: • Effect of 60 ppm*hr Cl{sub 2} gas on lung inflammation and mechanical function examined. • Pulmonary inflammation is transient and minor.

  12. Effects of COX-2 inhibitor in temporomandibular joint acute inflammation.

    Schütz, T C B; Andersen, M L; Tufik, S

    2007-05-01

    Since it is recognized that cyclo-oxygenase-2 mediates nociception and the sleep-wake cycle as well, and that acute inflammation of the temporomandibular joint (TMJ) results in sleep disturbances, we hypothesized that cyclo-oxygenase-2 inhibitor would restore the sleep pattern in this inflammatory rat model. First, sleep was monitored after the injection of Freund's adjuvant (FA group) or saline (SHAM group) into the rats' temporomandibular joint. Second, etoricoxib was co-administered in these groups. The Freund's adjuvant group showed a reduction in sleep efficiency, in rapid eye movement (REM), and in non-REM sleep, and an increase in sleep and REM sleep latency when compared with the SHAM group, while etoricoxib substantially increased sleep quality in the Freund's adjuvant group. These parameters returned progressively to those found in the SHAM group. Etoricoxib improved the sleep parameters, suggesting the involvement of the cyclo-oxygenase-2 enzyme in acute inflammation of the TMJ, specifically in REM sleep. PMID:17452571

  13. The Role of ischemia modified albumin in acute pulmonary embolism

    Zeynettin Kaya

    2014-01-01

    Full Text Available Background: Acute pulmonary embolism (PE is a life-threatening and a relatively common cardiovascular pathology. Although the pathogenesis of PE is well defined, there is no ideal diagnostic biochemical marker. Previous studies showed an increased ischemia modified albumin (IMA levels in acute PE; however, the relationship between IMA and right ventricular (RV dysfunction has not been examined. The aim of this study was to evaluate the diagnostic value of IMA and the relationship with RV dysfunction in acute PE. Materials and Methods : A total of 145 patients (70 females with suspected acute PE was enrolled to the study. Eighty-nine patients were diagnosed with acute PE via computed tomographic pulmonary angiography. Sixty-five patients with similar demographic and clinical characteristics were assigned to the control group. All patients were evaluated for RV dysfunction using transthoracic echocardiography. Results: Serum IMA levels were significantly increased in acute PE compared with control group (0.41 ± 0.06 vs. 0.34 ± 0.11, P = 0.001. There was no relationship between serum IMA levels and RV dysfunction. IMA levels were positively correlated with shock index and heart rate. Receiver operating curve analysis demonstrated that serum IMA levels higher than 0.4 put the diagnosis at sensitivity of 53.85% and at specificity of 85.96%. Conclusions: Although IMA levels are increased in patients with acute PE, it failed to predict RV dysfunction.

  14. Natural anticoagulants limit lipopolysaccharide-induced pulmonary coagulation but not inflammation

    Choi, G; Vlaar, A P J; Schouten, M; Van't Veer, C; van der Poll, T; Levi, M; Schultz, M J

    2007-01-01

    Pulmonary coagulopathy and hyperinflammation may contribute to an adverse outcome in sepsis. The present study determines the effects of natural inhibitors of coagulation on bronchoalveolar haemostasis and inflammation in a rat model of endotoxaemia. Male Sprague-Dawley rats were randomised to treat

  15. Effect of salbutamol on pulmonary responsiveness in chronic pulmonary allergic inflammation in guinea pigs

    Kasahara D.I.

    2005-01-01

    Full Text Available Beta-2-agonists have been widely used by asthmatic subjects to relieve their obstructive symptoms. However, there are reports that continuous use could lead to loss of bronchial protection and exacerbation of asthma symptoms. We evaluated the effect of two regimens of salbutamol administration (twice and five times a week in a model of chronic airway inflammation in male Hartley guinea pigs (protocol starting weight: 286 ± 30 g induced by repeated exposures to aerosols of ovalbumin (OVA. After sensitization, guinea pigs were exposed to aerosols of 0.1 mg/ml salbutamol solution twice a week (OVA + S2x, N = 7 or five times a week (OVA + S5x, N = 8. We studied allergen-specific (OVA inhalation time and -nonspecific (response to methacholine respiratory system responsiveness. Seventy-two hours after the last OVA challenge, guinea pigs were anesthetized and tracheostomized, respiratory system resistance and elastance were measured and a dose-response curve to inhaled methacholine chloride was obtained. Specific IgG1 was also quantified by the passive cutaneous anaphylactic technique. OVA-sensitized guinea pigs (N = 8 showed reduction of the time of OVA exposure before the onset of respiratory distress, at the 5th, 6th and 7th exposures (P < 0.001. The OVA + S2x group (but not the OVA + S5x group showed a significant increase in OVA inhalation time. There were no significant differences in pulmonary responsiveness to methacholine among the experimental groups. OVA + S2x (but not OVA + S5x animals showed a decrease in the levels of IgG1-specific anaphylactic antibodies compared to the OVA group (P < 0.05. Our results suggest that, in this experimental model, frequent administration of ß2-agonists results in a loss of some of their protective effects against the allergen.

  16. Global analysis of gene expression in pulmonary fibrosis reveals distinct programs regulating lung inflammation and fibrosis

    Kaminski, Naftali; Allard, John D.; Pittet, Jean F.; Zuo, Fengrong; Griffiths, Mark J. D.; Morris, David; Huang, Xiaozhu; Sheppard, Dean; Heller, Renu A.

    2000-02-01

    The molecular mechanisms of pulmonary fibrosis are poorly understood. We have used oligonucleotide arrays to analyze the gene expression programs that underlie pulmonary fibrosis in response to bleomycin, a drug that causes lung inflammation and fibrosis, in two strains of susceptible mice (129 and C57BL/6). We then compared the gene expression patterns in these mice with 129 mice carrying a null mutation in the epithelial-restricted integrin 6 subunit (6/-), which develop inflammation but are protected from pulmonary fibrosis. Cluster analysis identified two distinct groups of genes involved in the inflammatory and fibrotic responses. Analysis of gene expression at multiple time points after bleomycin administration revealed sequential induction of subsets of genes that characterize each response. The availability of this comprehensive data set should accelerate the development of more effective strategies for intervention at the various stages in the development of fibrotic diseases of the lungs and other organs.

  17. Effects of hydrogen sulfide on inflammation in caerulein-induced acute pancreatitis

    Bhatia Madhav

    2009-12-01

    Full Text Available Abstract Background Hydrogen sulfide (H2S, a gaseous mediator plays an important role in a wide range of physiological and pathological processes. H2S has been extensively studied for its various roles in cardiovascular and neurological disorders. However, the role of H2S in inflammation is still controversial. The current study was aimed to investigate the therapeutic potential of sodium hydrosulfide (NaHS, an H2S donor in in vivo model of acute pancreatitis in mice. Methods Acute pancreatitis was induced in mice by hourly caerulein injections (50 μg/kg for 10 hours. Mice were treated with different dosages of NaHS (5 mg/kg, 10 mg/kg or 15 mg/kg or with vehicle, distilled water (DW. NaHS or DW was administered 1 h before induction of pancreatitis. Mice were sacrificed 1 h after the last caerulein injection. Blood, pancreas and lung tissues were collected and were processed to measure the plasma amylase, myeloperoxidase (MPO activities in pancreas and lung and chemokines and adhesion molecules in pancreas and lung. Results It was revealed that significant reduction of inflammation, both in pancreas and lung was associated with NaHS 10 mg/kg. Further the anti-inflammatory effects of NaHS 10 mg/kg were associated with reduction of pancreatic and pulmonary inflammatory chemokines and adhesion molecules. NaHS 5 mg/kg did not cause significant improvement on inflammation in pancreas and associated lung injury and NaHS 15 mg/kg did not further enhance the beneficial effects seen with NaHS 10 mg/kg. Conclusion In conclusion, these data provide evidence for anti-inflammatory effects of H2S based on its dosage used.

  18. MDCT for the diagnosis of acute pulmonary embolism

    Schaefer-Prokop, C. [Dept. of Radiology, Academic Medical Center (AMC), Univ. of Amsterdam (Netherlands); Prokop, M. [Dept. of Radiology, Utrecht Medical Center (UMC), Univ. of Utrecht (Netherlands)

    2005-11-15

    With the advent of multidetector CT, pulmonary CT angiography (MD-CTPA) has substantially gained in spatial resolution and is the accepted method of choice to diagnose and rule out acute pulmonary embolism down to the subsegmental level. This article review means to optimize scanning technique and contrast injection protocols dependent on the scanner type used. It summarizes recent publications on the performance of MD-CTPA with special emphasis on the diagnostic accuracy, interpretation and clinical role of (isolated) peripheral emboli. Diagnostic algorithms are outlined that describe the role of CT in context with the pretest probability, the D-Dimer, lower limb sonography and scintigraphy. (orig.)

  19. Acute pulmonary embolism%急性肺栓塞

    Giancarlo Agnelli, M.D.; Cecilia Becattini, M.D., Ph.D.; 傅琳

    2010-01-01

    @@ 急性肺栓塞(acute pulmonary embolism, APE)的临床表现范围从休克(shock)或持续性低血压(sustained hypotension)到轻度呼吸困难(dyspnea).肺栓塞(pulmonary embolism)甚至有可能是无症状的,并且是在基于其他目的而实施的影像学操作中被诊断出来.APE的病死率范围从60%到<1%,取决于临床表现[1].抗凝是肺栓塞治疗的基础.

  20. Acute pulmonary oedema on the Ruwenzori mountain range.

    Naeije, R; Mélot, C.

    1990-01-01

    A 40 year old man had an episode of severe pulmonary oedema at 4000-5000 m during the ascent of the Margherita peak (5109 m) of Mount Stanley on the Ruwenzori. He had taken acetazolamide and high dose dexamethasone to treat symptoms of acute mountain sickness. Six years before he had been studied by right heart catheterisation as a healthy volunteer during hypoxic breathing at sea level. His pulmonary vascular reactivity had been within the normal range for 32 healthy subjects. This man had h...

  1. Computed tomography of acute pulmonary embolism: state-of-the-art

    Zhang, Long Jiang; Lu, Guang Ming [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Meinel, Felix G.; McQuiston, Andrew D.; Ravenel, James G. [Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States); Schoepf, U.J. [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States)

    2015-09-15

    Multidetector computed tomography (CT) plays an important role in the detection, risk stratification and prognosis evaluation of acute pulmonary embolism. This review will discuss the technical improvements for imaging peripheral pulmonary arteries, the methods of assessing pulmonary embolism severity based on CT findings, a multidetector CT technique for pulmonary embolism detection, and lastly, how to avoid overutilization of CT pulmonary angiography and overdiagnosis of pulmonary embolism. (orig.)

  2. Age-related differences in pulmonary effects of acute and subchronic episodic ozone exposures in Brown Norway rats.

    Snow, Samantha J; Gordon, Christopher J; Bass, Virginia L; Schladweiler, Mette C; Ledbetter, Allen D; Jarema, Kimberly A; Phillips, Pamela M; Johnstone, Andrew F; Kodavanti, Urmila P

    2016-06-01

    Ozone (O3) is known to induce adverse pulmonary and systemic health effects. Importantly, children and older persons are considered at-risk populations for O3-induced dysfunction, yet the mechanisms accounting for the age-related pulmonary responses to O3 are uncertain. In this study, we examined age-related susceptibility to O3 using 1 mo (adolescent), 4 mo (young adult), 12 mo (adult) and 24 mo (senescent) male Brown Norway rats exposed to filtered air or O3 (0.25 and 1.00 ppm), 6 h/day, two days/week for 1 week (acute) or 13 weeks (subchronic). Ventilatory function, assessed by whole-body plethysmography, and bronchoalveolar lavage fluid (BALF) biomarkers of injury and inflammation were used to examine O3-induced pulmonary effects. Relaxation time declined in all ages following the weekly exposures; however, this effect persisted only in the 24 mo rats following a five days recovery, demonstrating an inability to induce adaptation commonly seen with repeated O3 exposures. PenH was increased in all groups with an augmented response in the 4 mo rats following the subchronic O3 exposures. O3 led to increased breathing frequency and minute volume in the 1 and 4 mo animals. Markers of pulmonary permeability were increased in all age groups. Elevations in BALF γ-glutamyl transferase activity and lung inflammation following an acute O3 exposure were noted in only the 1 and 4 mo rats, which likely received an increased effective O3 dose. These data demonstrate that adolescent and young adult animals are more susceptible to changes in ventilation and pulmonary injury/inflammation caused by acute and episodic O3 exposure. PMID:27097751

  3. Airway inflammation in severe chronic obstructive pulmonary disease

    Very few studies have been made in-patient with severe chronic obstructive pulmonary disease and some of them carried out, have demonstrated an increment in the intensity of the inflammatory answer in the space and these patients' alveolar walls. However, there are not enough studies on the inflammatory answer in the small airway and in the lung glasses, object of the present study, comparing it with patient with light (COPD) or without COPD, in spite of similar history of smoker

  4. Acrolein exposure suppresses antigen-induced pulmonary inflammation

    Spiess, Page C; Kasahara, David; Habibovic, Aida; Hristova, Milena; Randall, Matthew J.; Poynter, Matthew E.; van der Vliet, Albert

    2013-01-01

    Background: Adverse health effects of tobacco smoke arise partly from its influence on innate and adaptive immune responses, leading to impaired innate immunity and host defense. The impact of smoking on allergic asthma remains unclear, with various reports demonstrating that cigarette smoke enhances asthma development but can also suppress allergic airway inflammation. Based on our previous findings that immunosuppressive effects of smoking may be largely attributed to one of its main reacti...

  5. Acute pulmonary alveolar proteinosis due to exposure to cotton dust

    Thind Gurcharan

    2009-01-01

    Full Text Available Secondary pulmonary alveolar proteinosis (PAP is rare but may occur in association with malignancy, certain infections, and exposure to inorganic or organic dust and some toxic fumes. This case report describes the second recorded case of PAP due to exposure to cotton dust. A 24-year-old man developed PAP after working as a spinner for eight years without respiratory protection. He was admitted as an emergency patient with very severe dyspnea for four months and cough for several years. Chest X-ray showed bilateral diffuse alveolar consolidation. He died 16 days later, and a diagnosis of acute pulmonary alveolar proteinosis was made at autopsy. The histopathology demonstrated alveoli and respiratory bronchioles filled with characteristic periodic acid Schiff-positive material, which also revealed birefringent bodies of cotton dust under polarized light. Secondary PAP can be fatal and present with acute respiratory failure. The occupational history and characteristic pathology can alert clinicians to the diagnosis.

  6. Sesame Oil Attenuates Ovalbumin-Induced Pulmonary Edema and Bronchial Neutrophilic Inflammation in Mice

    Dur-Zong Hsu

    2013-01-01

    Full Text Available Background. Allergic asthma is one of the most common chronic inflammatory diseases of airways. Severe asthma may lead to hospitalization and death. Sesame oil is a natural product with anti-inflammatory property. However, the effect of sesame oil on allergic asthma has never been studied. Objective. We investigate the effect of sesame oil on pulmonary inflammation in allergic asthma model. Methods. Allergic airway inflammation was induced by sensitizing with two doses of 10 mg ovalbumin (OVA and then challenged with 1% OVA nebulizer exposure (1 h/day for 3 days. Sesame oil (0.25, 0.5, or 1 mL/kg/day was given orally 30 min before each challenge. Samples were collected 24 h after the last challenge. Results. Data showed that sesame oil inhibited pulmonary edema and decreased interleukin (IL-1β and IL-6 levels in bronchoalveolar lavage fluid in OVA-treated mice. Sesame oil also decreased pulmonary nitrite level, inducible nitric oxide synthase expression, and neutrophil infiltration induced by OVA. Further, sesame oil decreased serum IgE level in OVA-treated mice. Conclusion. Sesame oil may attenuate pulmonary edema and bronchial neutrophilic inflammation by inhibiting systemic IgE level in allergic asthma.

  7. Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease

    Wedzicha, Wisia

    2014-01-01

    Simon E Brill, Jadwiga A Wedzicha Airway Disease Section, National Heart and Lung Institute, Imperial College, London, UK Abstract: Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in the history of this debilitating lung condition. Associated health care utilization and morbidity are high, and many patients require supplemental oxygen or ventilatory support. The last 2 decades have seen a substantial increase in our understanding of the best way to ma...

  8. Clinical Presentation of Acute Pulmonary Embolism: Survey of 800 Cases

    Miniati, M.; Cenci, C; Monti, S; D. Poli

    2012-01-01

    Background Pulmonary embolism (PE) is a common and potentially fatal disease that is still underdiagnosed. The objective of our study was to reappraise the clinical presentation of PE with emphasis on the identification of the symptoms and signs that prompt the patients to seek medical attention. Methodology/Principal Findings We studied 800 patients with PE from two different clinical settings: 440 were recruited in Pisa (Italy) as part of the Prospective Investigative Study of Acute Pulmona...

  9. Imaging diagnosis of acute pulmonary thromboembolism

    Pulmonary embolism (PE) is a frequent disease which requires an accurate diagnosis in order to establish an effective treatment considering that anticoagulant therapy may lead to complications. Lung ventilation / perfusion scintigraphy (LS V/Q) has been employed as the imaging meted of choice in patients with suspicion of PE. Pulmonary angiography is considered invasive, hence its utilization is usually reserved for otherwise unresolved cases. Other methods like venous Doppler ultrasound and echocardiography have a complementary role or are not widely indicated. The introduction of spiral CT (SCT), specially with multislice capabilities has made available a fast, relatively economic and efficient method for non-invasive diagnosis of PE. Availability of the technique is increasing and it has been included in some diagnostic algorithms for PE as the initial method of evaluation (and sometimes the only one). However, most research has been performed comparing this state-of-the-art technology with classical radionuclide protocols instead of using updated techniques such as SPECT and ultrafine radio aerosols. Moreover, SCT delivers much higher dose rates to the patient which must be taken into account specially in young individuals. In general, available evidence shows superior sensitivity of LS V/Q with higher specificity of SCT, within a context of similar overall accuracy provided optimized protocols are employed. Interpretation criteria for LS V/Q should be revised in an attempt to minimize indeterminate results, and together with the routine utilization of SPECT and novel ventilation systems should improve the performance of LS V/Q. The choice of the initial diagnostic modality should be guided by a correct determination of pre-test probability, clinical characteristics of the patient potentially influencing the efficacy and safety of the method, availability of the different techniques, relative costs and operator's experience. Such a selective and pragmatic

  10. The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation.

    Grabiec, Aleksander M; Hussell, Tracy

    2016-07-01

    Acute and chronic inflammatory responses in the lung are associated with the accumulation of large quantities of immune and structural cells undergoing apoptosis, which need to be engulfed by phagocytes in a process called 'efferocytosis'. Apoptotic cell recognition and removal from the lung is mediated predominantly by airway macrophages, though immature dendritic cells and non-professional phagocytes, such as epithelial cells and mesenchymal cells, can also display this function. Efficient clearance of apoptotic cells from the airways is essential for successful resolution of inflammation and the return to lung homeostasis. Disruption of this process leads to secondary necrosis of accumulating apoptotic cells, release of necrotic cell debris and subsequent uncontrolled inflammatory activation of the innate immune system by the released 'damage associated molecular patterns' (DAMPS). To control the duration of the immune response and prevent autoimmune reactions, anti-inflammatory signalling cascades are initiated in the phagocyte upon apoptotic cell uptake, mediated by a range of receptors that recognise specific phospholipids or proteins externalised on, or secreted by, the apoptotic cell. However, prolonged activation of apoptotic cell recognition receptors, such as the family of receptor tyrosine kinases Tyro3, Axl and MerTK (TAM), may delay or prevent inflammatory responses to subsequent infections. In this review, we will discuss recent advances in our understanding of the mechanism controlling apoptotic cell recognition and removal from the lung in homeostasis and during inflammation, the contribution of defective efferocytosis to chronic inflammatory lung diseases, such as chronic obstructive pulmonary disease, asthma and cystic fibrosis, and implications of the signals triggered by apoptotic cells in the susceptibility to pulmonary microbial infections. PMID:26957481

  11. Hypoxic pulmonary vasoconstriction as a contributor to response in acute pulmonary embolism.

    Burrowes, K S; Clark, A R; Wilsher, M L; Milne, D G; Tawhai, M H

    2014-08-01

    Hypoxic pulmonary vasoconstriction (HPV) is an adaptive response unique to the lung whereby blood flow is diverted away from areas of low alveolar oxygen to improve ventilation-perfusion matching and resultant gas exchange. Some previous experimental studies have suggested that the HPV response to hypoxia is blunted in acute pulmonary embolism (APE), while others have concluded that HPV contributes to elevated pulmonary blood pressures in APE. To understand these contradictory observations, we have used a structure-based computational model of integrated lung function in 10 subjects to study the impact of HPV on pulmonary hemodynamics and gas exchange in the presence of regional arterial occlusion. The integrated model includes an experimentally-derived model for HPV. Its function is validated against measurements of pulmonary vascular resistance in normal subjects at four levels of inspired oxygen. Our results show that the apparently disparate observations of previous studies can be explained within a single model: the model predicts that HPV increases mean pulmonary artery pressure in APE (by 8.2 ± 7.0% in these subjects), and concurrently shows a reduction in response to hypoxia in the subjects who have high levels of occlusion and therefore maximal HPV in normoxia. PMID:24770844

  12. Hyaluronan fragments as mediators of inflammation in allergic pulmonary disease.

    Ghosh, Sumit; Hoselton, Scott A; Dorsam, Glenn P; Schuh, Jane M

    2015-05-01

    Asthma is frequently caused and/or exacerbated by sensitization to allergens, which are ubiquitous in many indoor and outdoor environments. Severe asthma is characterized by airway hyperresponsiveness and bronchial constriction in response to an inhaled allergen, leading to a disease course that is often very difficult to treat with standard asthma therapies. As a result of interactions among inflammatory cells, structural cells, and the intercellular matrix of the allergic lung, patients with sensitization to allergens may experience a greater degree of tissue injury followed by airway wall remodeling and progressive, accumulated pulmonary dysfunction as part of the disease sequela. In addition, turnover of extracellular matrix (ECM) components is a hallmark of tissue injury and repair. This review focuses on the role of the glycosaminoglycan hyaluronan (HA), a component of the ECM, in pulmonary injury and repair with an emphasis on allergic asthma. Both the synthesis and degradation of the ECM are critical contributors to tissue repair and remodeling. Fragmented HA accumulates during tissue injury and functions in ways distinct from the larger native polymer. There is gathering evidence that HA degradation products are active participants in stimulating the expression of inflammatory genes in a variety of immune cells at the injury site. In this review, we will consider recent advances in the understanding of the mechanisms that are associated with HA accumulation and inflammatory cell recruitment in the asthmatic lung. PMID:25582403

  13. Pulmonary Inflammation Triggered by Ricin Toxin Requires Macrophages and IL-1 Signaling1

    Lindauer, Meghan L.; Wong, John; Iwakura, Yoichiro; Magun, Bruce E

    2009-01-01

    Ricin is a potent ribotoxin considered to be a potentially dangerous bioterrorist agent due to its wide availability and the possibility of aerosol delivery to human populations. Studies in rodents and nonhuman primates have demonstrated that ricin delivered to the pulmonary system leads to acute lung injury and symptoms resembling acute respiratory distress syndrome. Increasing evidence suggests that the inflammatory effects triggered by ricin are responsible for its lethality. We demonstrat...

  14. Acute pulmonary admissions following implementation of a national workplace smoking ban.

    Kent, Brian D

    2012-09-01

    The implementation of workplace smoking bans has contributed to a significant reduction in the incidence of acute coronary syndrome admissions, but their influence on adult acute pulmonary disease admissions is unclear. We sought to assess the impact of a national smoking ban on nationwide admissions of individuals of working age with acute pulmonary illness.

  15. Acute phase response, inflammation and metabolic syndrome biomarkers of Libby asbestos exposure

    Shannahan, Jonathan H. [Curriculum in Toxicology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599 (United States); Alzate, Oscar [Systems Proteomics Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599 (United States); Winnik, Witold M.; Andrews, Debora [Proteomics Core, Research Core Unit, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 (United States); Schladweiler, Mette C. [Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 (United States); Ghio, Andrew J. [Clinical Research Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Chapel Hill, NC 27599 (United States); Gavett, Stephen H. [Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 (United States); Kodavanti, Urmila P., E-mail: Kodavanti.Urmila@epa.gov [Cardiopulmonary and Immunotoxicology Branch, Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711 (United States)

    2012-04-15

    Identification of biomarkers assists in the diagnosis of disease and the assessment of health risks from environmental exposures. We hypothesized that rats exposed to Libby amphibole (LA) would present with a unique serum proteomic profile which could help elucidate epidemiologically-relevant biomarkers. In four experiments spanning varied protocols and temporality, healthy (Wistar Kyoto, WKY; and F344) and cardiovascular compromised (CVD) rat models (spontaneously hypertensive, SH; and SH heart failure, SHHF) were intratracheally instilled with saline (control) or LA. Serum biomarkers of cancer, inflammation, metabolic syndrome (MetS), and the acute phase response (APR) were analyzed. All rat strains exhibited acute increases in α-2-macroglobulin, and α1-acid glycoprotein. Among markers of inflammation, lipocalin-2 was induced in WKY, SH and SHHF and osteopontin only in WKY after LA exposure. While rat strain- and age-related changes were apparent in MetS biomarkers, no LA effects were evident. The cancer marker mesothelin was increased only slightly at 1 month in WKY in one of the studies. Quantitative Intact Proteomic profiling of WKY serum at 1 day or 4 weeks after 4 weekly LA instillations indicated no oxidative protein modifications, however APR proteins were significantly increased. Those included serine protease inhibitor, apolipoprotein E, α-2-HS-glycoprotein, t-kininogen 1 and 2, ceruloplasmin, vitamin D binding protein, serum amyloid P, and more 1 day after last LA exposure. All changes were reversible after a short recovery regardless of the acute or long-term exposures. Thus, LA exposure induces an APR and systemic inflammatory biomarkers that could have implications in systemic and pulmonary disease in individuals exposed to LA. -- Highlights: ► Biomarkers of asbestos exposure are required for disease diagnosis. ► Libby amphibole exposure is associated with increased human mortality. ► Libby amphibole increases circulating proteins involved

  16. Acute phase response, inflammation and metabolic syndrome biomarkers of Libby asbestos exposure

    Identification of biomarkers assists in the diagnosis of disease and the assessment of health risks from environmental exposures. We hypothesized that rats exposed to Libby amphibole (LA) would present with a unique serum proteomic profile which could help elucidate epidemiologically-relevant biomarkers. In four experiments spanning varied protocols and temporality, healthy (Wistar Kyoto, WKY; and F344) and cardiovascular compromised (CVD) rat models (spontaneously hypertensive, SH; and SH heart failure, SHHF) were intratracheally instilled with saline (control) or LA. Serum biomarkers of cancer, inflammation, metabolic syndrome (MetS), and the acute phase response (APR) were analyzed. All rat strains exhibited acute increases in α-2-macroglobulin, and α1-acid glycoprotein. Among markers of inflammation, lipocalin-2 was induced in WKY, SH and SHHF and osteopontin only in WKY after LA exposure. While rat strain- and age-related changes were apparent in MetS biomarkers, no LA effects were evident. The cancer marker mesothelin was increased only slightly at 1 month in WKY in one of the studies. Quantitative Intact Proteomic profiling of WKY serum at 1 day or 4 weeks after 4 weekly LA instillations indicated no oxidative protein modifications, however APR proteins were significantly increased. Those included serine protease inhibitor, apolipoprotein E, α-2-HS-glycoprotein, t-kininogen 1 and 2, ceruloplasmin, vitamin D binding protein, serum amyloid P, and more 1 day after last LA exposure. All changes were reversible after a short recovery regardless of the acute or long-term exposures. Thus, LA exposure induces an APR and systemic inflammatory biomarkers that could have implications in systemic and pulmonary disease in individuals exposed to LA. -- Highlights: ► Biomarkers of asbestos exposure are required for disease diagnosis. ► Libby amphibole exposure is associated with increased human mortality. ► Libby amphibole increases circulating proteins involved

  17. Phagocyte respiratory burst activates macrophage erythropoietin signalling to promote acute inflammation resolution.

    Luo, Bangwei; Wang, Jinsong; Liu, Zongwei; Shen, Zigang; Shi, Rongchen; Liu, Yu-Qi; Liu, Yu; Jiang, Man; Wu, Yuzhang; Zhang, Zhiren

    2016-01-01

    Inflammation resolution is an active process, the failure of which causes uncontrolled inflammation which underlies many chronic diseases. Therefore, endogenous pathways that regulate inflammation resolution are fundamental and of wide interest. Here, we demonstrate that phagocyte respiratory burst-induced hypoxia activates macrophage erythropoietin signalling to promote acute inflammation resolution. This signalling is activated following acute but not chronic inflammation. Pharmacological or genetical inhibition of the respiratory burst suppresses hypoxia and macrophage erythropoietin signalling. Macrophage-specific erythropoietin receptor-deficient mice and chronic granulomatous disease (CGD) mice, which lack the capacity for respiratory burst, display impaired inflammation resolution, and exogenous erythropoietin enhances this resolution in WT and CGD mice. Mechanistically, erythropoietin increases macrophage engulfment of apoptotic neutrophils via PPARγ, promotes macrophage removal of debris and enhances macrophage migration to draining lymph nodes. Together, our results provide evidences of an endogenous pathway that regulates inflammation resolution, with important implications for treating inflammatory conditions. PMID:27397585

  18. Relationship between airway inflammation and remodeling in patients with asthma and chronic obstructive pulmonary disease

    Górska K; Krenke R; Kosciuch J; Korczynski P; Zukowska M; Domagala-Kulawik J; Maskey-Warzechowska M; Chazan R

    2009-01-01

    Abstract Despite a number of important differences in the pathogenesis, course and prognosis of asthma and chronic obstructive pulmonary disease (COPD), these two entities also have common features with airway inflammation being one of them. Airway remodeling is a characteristic feature of asthma, but data on the bronchial wall thickening in COPD patients are still scarce. Aim To assess the relation between the inflammatory cell count in the bronchoalveolar lavage fluid (BALF) and thickness o...

  19. The Role of Sphingolipids and Ceramide in Pulmonary Inflammation in Cystic Fibrosis

    Becker, Katrin Anne; Riethmüller, Joachim; Zhang, Yang; Gulbins, Erich

    2010-01-01

    Sphingolipids and in particular ceramide have been shown to be critically involved in the response to many receptor-mediated, but also receptor-independent, mainly stress stimuli. Recent studies demonstrate that ceramide plays an important role in the pathogenesis of cystic fibrosis, a hereditary metabolic disorder caused by mutations of the Cystic Fibrosis Transmembrane Conductance Regulator. Patients with cystic fibrosis suffer from chronic pulmonary inflammation and microbial lung infectio...

  20. IL-17A is essential to the development of elastase-induced pulmonary inflammation and emphysema in mice

    Kurimoto Etsuko; Miyahara Nobuaki; Kanehiro Arihiko; Waseda Koichi; Taniguchi Akihiko; Ikeda Genyo; Koga Hikari; Nishimori Hisakazu; Tanimoto Yasushi; Kataoka Mikio; Iwakura Yoichiro; Gelfand Erwin W; Tanimoto Mitsune

    2013-01-01

    Abstract Background Pulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. Although IL-17A contributes to many chronic inflammatory diseases, it’s role in the inflammatory response of elastase-induced emphysema remains unclear. Methods In a model of elastase-induced pulmonary emphysema we examined the response of IL-17A-deficient mice, monitoring airway inflammation, static compliance, lung histology and levels of neutrophil-related chemokine ...

  1. [Acute massive pulmonary embolism in a patient using clavis panax].

    Yüksel, Isa Oner; Arslan, Sakir; Cağırcı, Göksel; Yılmaz, Akar

    2013-06-01

    In recent years, the use of herbal combinations, plant extracts or food supplements has increased in our country and all over the world. However, there is not enough data to determine the effective doses of these substances in the composition of herbal preparations, or their effects on metabolism and drug interactions. With the widespread use of herbal combinations, life-threatening side effects and clinical manifestations that arise from them have been reported. Herein we present a case with acute massive pulmonary embolism while using an herbal combination in the context of Tribulus terrestris, Avena sativa and Panax ginseng. A 41-year-old man was admitted to the emergency department with the complaint of sudden onset of dyspnea and syncope. As a result of investigations (blood gases, echocardiography, ventilation-perfusion scintigraphy) he was diagnosed with an acute massive pulmonary embolism. The patient's use of panax did not pose as a risk factor for the pulmonary embolism. He was given thrombolytic therapy and shortness of breath improved. At the pre-discharge the patient was informed of the risks associated with the herbal combination, especially panax. Coumadin was started and he was discharged for the INR checks to come. PMID:23760126

  2. Pulmonary and pleural inflammation after intratracheal instillation of short single-walled and multi-walled carbon nanotubes.

    Fujita, Katsuhide; Fukuda, Makiko; Endoh, Shigehisa; Maru, Junko; Kato, Haruhisa; Nakamura, Ayako; Shinohara, Naohide; Uchino, Kanako; Honda, Kazumasa

    2016-08-22

    Relationships between the physical properties of carbon nanotubes (CNTs) and their toxicities have been studied. However, little research has been conducted to investigate the pulmonary and pleural inflammation caused by short-fiber single-walled CNTs (SWCNTs) and multi-walled CNTs (MWCNTs). This study was performed to characterize differences in rat pulmonary and pleural inflammation caused by intratracheal instillation with doses of 0.15 or 1.5mg/kg of either short-sized SWCNTs or MWCNTs. Data from bronchoalveolar lavage fluid analysis, histopathological findings, and transcriptional profiling of rat lungs obtained over a 90-day period indicated that short SWCNTs caused persistent pulmonary inflammation. In addition, the short MWCNTs markedly impacted alveoli immediately after instillation, with the levels of pulmonary inflammation following MWCNT instillation being reduced in a time-dependent manner. MWCNT instillation induced greater levels of pleural inflammation than did short SWCNTs. SWCNTs and MWCNTs translocated in mediastinal lymph nodes were observed, suggesting that SWCNTs and MWCNTs underwent lymphatic drainage to the mediastinal lymph nodes after pleural penetration. Our results suggest that short SWCNTs and MWCNTs induced pulmonary and pleural inflammation and that they might be transported throughout the body after intratracheal instillation. The extent of changes in inflammation differed following SWCNT and MWCNT instillation in a time-dependent manner. PMID:27259835

  3. Surgical treatment of acute pulmonary embolism--a 12-year retrospective analysis

    Lehnert, Per; Møller, Christian H; Carlsen, Jørn;

    2012-01-01

    Surgical embolectomy for acute pulmonary embolism (PE) is considered to be a high risk procedure and therefore a last treatment option. We wanted to evaluate the procedures role in modern treatment of acute PE.......Surgical embolectomy for acute pulmonary embolism (PE) is considered to be a high risk procedure and therefore a last treatment option. We wanted to evaluate the procedures role in modern treatment of acute PE....

  4. Systemic Inflammation in Chronic Obstructive Pulmonary Disease: May Adipose Tissue Play a Role? Review of the Literature and Future Perspectives

    Ruzena Tkacova

    2010-01-01

    Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Low-grade systemic inflammation is considered a hallmark of COPD that potentially links COPD to increased rate of systemic manifestations of the disease. Obesity with/without the metabolic syndrome and cachexia represent two poles of metabolic abnormalities that may relate to systemic inflammation. On one hand systemic inflammatory syndrome likely reflects inflammation in the lungs, i.e. result...

  5. Severity assessment of acute pulmonary embolism: evaluation using helical CT

    The objective was to evaluate the helical CT (HCT) criteria that could indicate severe pulmonary embolism (PE). In a retrospective study, 81 patients (mean age 62 years) with clinical suspicion of PE explored by HCT were studied. The patients were separated into three different groups according to clinical severity and treatment decisions: group SPE included patients with severe PE based on clinical data who were treated by fibrinolysis or embolectomy (n=20); group NSPE included patients with non-severe PE who received heparin (n=30); and group WPE included patients without PE (n=31). For each patient we calculated a vascular obstruction index based on the site of obstruction and the degree of occlusion in the pulmonary artery. We noted the HCT signs, i.e., cardiac and pulmonary artery dimensions, that could indicate acute cor pulmonale. According to multivariate analysis, factors significantly correlated with the severity of PE were: the vascular obstruction index (group SPE: 54%; group NSPE: 24%; p<0.001); the maximum minor axis of the left ventricle (group SPE: 30.2 mm; group NSPE: 40.4 mm; p<0.001); the diameter of the central pulmonary artery (group SPE: 32.4 mm; group NSPE: 28.3 mm; p<0.001); the maximum minor axis of the right ventricle (group SPE: 47.5 mm; group NSPE: 42.7 mm; p=0.029); the right ventricle/left ventricle minor axis ratio (group SPE: 1.63; group NSPE: 1.09; p<0.0001). Our data suggest that hemodynamic severity of PE can be assessed on HCT scans by measuring four main criteria: the vascular obstruction index; the minimum diameter of the left ventricle; the RV:LV ratio; and the diameter of the central pulmonary artery. (orig.)

  6. Echocardiographic changes during acute pulmonary edema subsequent to scorpion sting

    K Delma

    2012-01-01

    Full Text Available Acute pulmonary edema (APE occurring after scorpion sting is the leading cause of death of the victims of scorpion envenomation. The APE origin is still questioned by physicians treating these patients. Based on echocardiographic study of 20 patients with severe envenomation treated in Ouargla Hospital resuscitation ward during the last four years, the APE etiology seems more likely cardiogenic, referring to cardiac symptoms confirmed by echocardiography although other mechanisms may also be involved. This hypothesis is further confirmed by the positive response of patients to the administration of dobutamine.

  7. Pharmacological characterisation of anti-inflammatory compounds in acute and chronic mouse models of cigarette smoke-induced inflammation

    Mok Joanie

    2010-09-01

    Full Text Available Abstract Background Candidate compounds being developed to treat chronic obstructive pulmonary disease are typically assessed using either acute or chronic mouse smoking models; however, in both systems compounds have almost always been administered prophylactically. Our aim was to determine whether the prophylactic effects of reference anti-inflammatory compounds in acute mouse smoking models reflected their therapeutic effects in (more clinically relevant chronic systems. Methods To do this, we started by examining the type of inflammatory cell infiltrate which occurred after acute (3 days or chronic (12 weeks cigarette smoke exposure (CSE using female, C57BL/6 mice (n = 7-10. To compare the effects of anti-inflammatory compounds in these models, mice were exposed to either 3 days of CSE concomitant with compound dosing or 14 weeks of CSE with dosing beginning after week 12. Budesonide (1 mg kg-1; i.n., q.d., roflumilast (3 mg kg-1; p.o., q.d. and fluvastatin (2 mg kg-1; p.o., b.i.d. were dosed 1 h before (and 5 h after for fluvastatin CSE. These dose levels were selected because they have previously been shown to be efficacious in mouse models of lung inflammation. Bronchoalveolar lavage fluid (BALF leukocyte number was the primary endpoint in both models as this is also a primary endpoint in early clinical studies. Results To start, we confirmed that the inflammatory phenotypes were different after acute (3 days versus chronic (12 weeks CSE. The inflammation in the acute systems was predominantly neutrophilic, while in the more chronic CSE systems BALF neutrophils (PMNs, macrophage and lymphocyte numbers were all increased (p Conclusions These results demonstrate that the acute, prophylactic systems can be used to identify compounds with therapeutic potential, but may not predict a compound's efficacy in chronic smoke exposure models.

  8. [Acute pulmonary embolism: beware of the wolf in sheep's clothing].

    Klok, Frederikus A; Vahl, Jelmer E; Huisman, Menno V; van Dijkman, Paul R M

    2012-01-01

    Two male patients aged 57 and 73 were referred to the cardiologist because of progressive dyspnoea. In one patient, the general practitioner had previously adopted an expectative policy because of a clean chest X-ray. At presentation after 4 weeks, the patient was diagnosed with and treated for acute coronary syndrome because of minor ECG abnormalities. Additional CT scanning showed a large saddle embolus. Despite adequate treatment, the patient suffered an electrical asystole and died. The other patient underwent ECG, bicycle ergometry, MRI adenosine, echocardiography and lung function tests over a period of 5 weeks before pulmonary embolism (PE) was diagnosed. As the signs and symptoms of PE are largely non-specific, diagnostic delay is common, with risk of poor clinical outcome. PE should at least be considered whenever a patient presents with acute or worsening breathlessness, chest pain, circulatory collapse or coughing, particularly in the presence of known thrombotic risk factors or when there is no clear alternative. PMID:22296892

  9. Medical image of the week: acute amiodarone pulmonary toxicity

    Mazursky K

    2015-10-01

    Full Text Available No abstract available. Article truncated after 150 words. A 71 year old man with a medical history significant for chronic obstructive pulmonary disease, coronary artery disease with post-operative status coronary artery bypass grafting, heart failure with reduced ejection fraction (25% and atrial fibrillation/flutter underwent an elective ablation of the tachyarrhythmia at another facility and was prescribed amiodarone post procedure. He started complaining of cough and dyspnea one day post procedure and was empirically treated with 2 weeks of broad spectrum antibiotics. He subsequently was transferred to our facility due to worsening symptoms. He also complained of nausea, anorexia with resultant weight loss since starting amiodarone, which was stopped 5 days prior to transfer. Infectious work up was negative. On arrival to our facility, he was diagnosed with small sub-segmental pulmonary emboli, pulmonary edema and possible acute amiodarone toxicity. His was profoundly hypoxic requiring high flow nasal cannula or 100% non-rebreather mask at all times. His symptoms persisted despite ...

  10. Acute pulmonary embolism during an endoscopic retrograde cholangiopancreatography

    Nate P Painter

    2014-01-01

    Full Text Available A 76-year-old female patient presented for an endoscopic retrograde cholangiopancreatography (ERCP for the removal of a biliary stent and lithotripsy. During the procedure, an acute drop in the end-tidal CO 2 , followed by cardiovascular collapse prompted the initiation of the advanced cardiac life support protocol. Transesophageal echocardiography (TEE demonstrated direct evidence of pulmonary embolism. The patient was promptly treated with thrombolytic therapy and subsequently discharged home on oral warfarin therapy, with no noted sequelae. Although, there have been case reports of air embolism during an ERCP presenting with cardiovascular collapse, to the best of our knowledge, there are no reported cases of acute pulmonary embolus during this procedure. While the availability of TEE in the operating suites is quite common, quick access and interpretation capabilities in remote locations may not be as common. With the expansion of anesthesia services outside of the operating rooms, it may be prudent to develop rapid response systems that incorporate resources such as TEE and trained personnel to deal with such emergent situations.

  11. Acute pulmonary embolism during an endoscopic retrograde cholangiopancreatography.

    Painter, Nate P; Kumar, Priya A; Arora, Harendra

    2014-01-01

    A 76-year-old female patient presented for an endoscopic retrograde cholangiopancreatography (ERCP) for the removal of a biliary stent and lithotripsy. During the procedure, an acute drop in the end-tidal CO 2 , followed by cardiovascular collapse prompted the initiation of the advanced cardiac life support protocol. Transesophageal echocardiography (TEE) demonstrated direct evidence of pulmonary embolism. The patient was promptly treated with thrombolytic therapy and subsequently discharged home on oral warfarin therapy, with no noted sequelae. Although, there have been case reports of air embolism during an ERCP presenting with cardiovascular collapse, to the best of our knowledge, there are no reported cases of acute pulmonary embolus during this procedure. While the availability of TEE in the operating suites is quite common, quick access and interpretation capabilities in remote locations may not be as common. With the expansion of anesthesia services outside of the operating rooms, it may be prudent to develop rapid response systems that incorporate resources such as TEE and trained personnel to deal with such emergent situations. PMID:24732617

  12. Investigating suspected acute pulmonary embolism - what are hospital clinicians thinking?

    McQueen, A.S. [Department of Radiology, Royal Victoria Infirmary, Newcastle upon Tyne (United Kingdom)], E-mail: andrewmcqueen7@hotmail.com; Worthy, S. [Department of Radiology, Royal Victoria Infirmary, Newcastle upon Tyne (United Kingdom); Keir, M.J. [Department of Medical Physics, Royal Victoria Infirmary, Newcastle upon Tyne (United Kingdom)

    2008-06-15

    Aims: To assess local clinical knowledge of the appropriate investigation of suspected acute pulmonary embolism (PE) and this compare with the 2003 British Thoracic Society (BTS) guidelines as a national reference standard. Methods: A clinical questionnaire was produced based on the BTS guidelines. One hundred and eight-six participants completed the questionnaires at educational sessions for clinicians of all grades, within a single NHS Trust. The level of experience amongst participants ranged from final year medical students to consultant physicians. Results: The clinicians were divided into four groups based on seniority: Pre-registration, Junior, Middle, and Senior. Forty-six point eight percent of all the clinicians correctly identified three major risk factors for PE and 25.8% recognized the definition of the recommended clinical probability score from two alternatives. Statements regarding the sensitivity of isotope lung imaging and computed tomography pulmonary angiography (CTPA) received correct responses from 41.4 and 43% of participants, respectively, whilst 81.2% recognized that an indeterminate ventilation-perfusion scintigraphy (V/Q) study requires further imaging. The majority of clinicians correctly answered three clinical scenario questions regarding use of D-dimers and imaging (78, 85, and 57.5%). There was no statistically significant difference between the four groups for any of the eight questions. Conclusions: The recommended clinical probability score was unfamiliar to all four groups of clinicians in the present study, and the majority of doctors did not agree that a negative CTPA or isotope lung scintigraphy reliably excluded PE. However, questions based on clinical scenarios received considerably higher rates of correct responses. The results indicate that various aspects of the national guidelines on suspected acute pulmonary embolism are unfamiliar to many UK hospital clinicians. Further research is needed to identify methods to improve

  13. Investigating suspected acute pulmonary embolism - what are hospital clinicians thinking?

    Aims: To assess local clinical knowledge of the appropriate investigation of suspected acute pulmonary embolism (PE) and this compare with the 2003 British Thoracic Society (BTS) guidelines as a national reference standard. Methods: A clinical questionnaire was produced based on the BTS guidelines. One hundred and eight-six participants completed the questionnaires at educational sessions for clinicians of all grades, within a single NHS Trust. The level of experience amongst participants ranged from final year medical students to consultant physicians. Results: The clinicians were divided into four groups based on seniority: Pre-registration, Junior, Middle, and Senior. Forty-six point eight percent of all the clinicians correctly identified three major risk factors for PE and 25.8% recognized the definition of the recommended clinical probability score from two alternatives. Statements regarding the sensitivity of isotope lung imaging and computed tomography pulmonary angiography (CTPA) received correct responses from 41.4 and 43% of participants, respectively, whilst 81.2% recognized that an indeterminate ventilation-perfusion scintigraphy (V/Q) study requires further imaging. The majority of clinicians correctly answered three clinical scenario questions regarding use of D-dimers and imaging (78, 85, and 57.5%). There was no statistically significant difference between the four groups for any of the eight questions. Conclusions: The recommended clinical probability score was unfamiliar to all four groups of clinicians in the present study, and the majority of doctors did not agree that a negative CTPA or isotope lung scintigraphy reliably excluded PE. However, questions based on clinical scenarios received considerably higher rates of correct responses. The results indicate that various aspects of the national guidelines on suspected acute pulmonary embolism are unfamiliar to many UK hospital clinicians. Further research is needed to identify methods to improve

  14. Whole blood viscosity assessment issues IV: Prevalence in acute phase inflammation

    Ezekiel Uba Nwose

    2010-08-01

    Full Text Available Background: Hyperviscosity syndrome has been suggested as not simply an acute reaction. Yet, erythrocyte sedimentation rate is associated with whole blood viscosity and it is an indirect acute phase inflammation marker. Aims: This work investigates the prevalence of hyperviscosity in acute phase inflammation. Materials and Methods: Archived clinical pathology data for the period of 1999 to 2008 were utilized. 40,632-cases tested for C-reactive protein and/or erythrocyte sedimentation rate from five alternate years, which were concomitantly tested for haematocrit and total proteins, were extracted. The prevalence of abnormal viscosity associated with positive results of C-reactive protein and erythrocyte sedimentation rate were evaluated. Results: Hyperviscosity is infrequently associated with positive C-reactive protein (2.9% and erythrocyte sedimentation rate (2.7% sub-populations, and are not statistically different from their respective negative sub-populations. Normoviscosity is significantly more prevalent in the positive sub-populations (p < 0.01. Further analyses indicate that prevalence of acute phase inflammation is statistically significantly less in hyperviscosity compared to normoviscosity sub-population (p < 0.00001. Actual blood viscosity level increases with level of inflammation though. Conclusion: The study demonstrates that although blood viscosity level may increase with inflammation, hyperviscosity is not frequent in, or sensitive to acute phase inflammation. It portends that whole blood viscosity is not unspecific as acute phase inflammation markers. It calls for clinicians to consider utilizing whole blood viscosity in disease conditions where stasis is implicated, in which it is specific and valuable. It would also benefit to establish whether hyperviscosity is a chronic phase inflammation marker.

  15. Attenuation of acute nitrogen mustard-induced lung injury, inflammation and fibrogenesis by a nitric oxide synthase inhibitor

    Malaviya, Rama; Venosa, Alessandro [Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States); Hall, LeRoy [Drug Safety Sciences, Johnson and Johnson, Raritan, NJ 08869 (United States); Gow, Andrew J. [Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States); Sinko, Patrick J. [Department of Pharmaceutics, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States); Laskin, Jeffrey D. [Department of Environmental and Occupational Medicine, UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ 08854 (United States); Laskin, Debra L., E-mail: laskin@eohsi.rutgers.edu [Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States)

    2012-12-15

    Nitrogen mustard (NM) is a toxic vesicant known to cause damage to the respiratory tract. Injury is associated with increased expression of inducible nitric oxide synthase (iNOS). In these studies we analyzed the effects of transient inhibition of iNOS using aminoguanidine (AG) on NM-induced pulmonary toxicity. Rats were treated intratracheally with 0.125 mg/kg NM or control. Bronchoalveolar lavage fluid (BAL) and lung tissue were collected 1 d–28 d later and lung injury, oxidative stress and fibrosis assessed. NM exposure resulted in progressive histopathological changes in the lung including multifocal lesions, perivascular and peribronchial edema, inflammatory cell accumulation, alveolar fibrin deposition, bronchiolization of alveolar septal walls, and fibrosis. This was correlated with trichrome staining and expression of proliferating cell nuclear antigen (PCNA). Expression of heme oxygenase (HO)-1 and manganese superoxide dismutase (Mn-SOD) was also increased in the lung following NM exposure, along with levels of protein and inflammatory cells in BAL, consistent with oxidative stress and alveolar-epithelial injury. Both classically activated proinflammatory (iNOS{sup +} and cyclooxygenase-2{sup +}) and alternatively activated profibrotic (YM-1{sup +} and galectin-3{sup +}) macrophages appeared in the lung following NM administration; this was evident within 1 d, and persisted for 28 d. AG administration (50 mg/kg, 2 ×/day, 1 d–3 d) abrogated NM-induced injury, oxidative stress and inflammation at 1 d and 3 d post exposure, with no effects at 7 d or 28 d. These findings indicate that nitric oxide generated via iNOS contributes to acute NM-induced lung toxicity, however, transient inhibition of iNOS is not sufficient to protect against pulmonary fibrosis. -- Highlights: ► Nitrogen mustard (NM) induces acute lung injury and fibrosis. ► Pulmonary toxicity is associated with increased expression of iNOS. ► Transient inhibition of iNOS attenuates acute

  16. Attenuation of acute nitrogen mustard-induced lung injury, inflammation and fibrogenesis by a nitric oxide synthase inhibitor

    Nitrogen mustard (NM) is a toxic vesicant known to cause damage to the respiratory tract. Injury is associated with increased expression of inducible nitric oxide synthase (iNOS). In these studies we analyzed the effects of transient inhibition of iNOS using aminoguanidine (AG) on NM-induced pulmonary toxicity. Rats were treated intratracheally with 0.125 mg/kg NM or control. Bronchoalveolar lavage fluid (BAL) and lung tissue were collected 1 d–28 d later and lung injury, oxidative stress and fibrosis assessed. NM exposure resulted in progressive histopathological changes in the lung including multifocal lesions, perivascular and peribronchial edema, inflammatory cell accumulation, alveolar fibrin deposition, bronchiolization of alveolar septal walls, and fibrosis. This was correlated with trichrome staining and expression of proliferating cell nuclear antigen (PCNA). Expression of heme oxygenase (HO)-1 and manganese superoxide dismutase (Mn-SOD) was also increased in the lung following NM exposure, along with levels of protein and inflammatory cells in BAL, consistent with oxidative stress and alveolar-epithelial injury. Both classically activated proinflammatory (iNOS+ and cyclooxygenase-2+) and alternatively activated profibrotic (YM-1+ and galectin-3+) macrophages appeared in the lung following NM administration; this was evident within 1 d, and persisted for 28 d. AG administration (50 mg/kg, 2 ×/day, 1 d–3 d) abrogated NM-induced injury, oxidative stress and inflammation at 1 d and 3 d post exposure, with no effects at 7 d or 28 d. These findings indicate that nitric oxide generated via iNOS contributes to acute NM-induced lung toxicity, however, transient inhibition of iNOS is not sufficient to protect against pulmonary fibrosis. -- Highlights: ► Nitrogen mustard (NM) induces acute lung injury and fibrosis. ► Pulmonary toxicity is associated with increased expression of iNOS. ► Transient inhibition of iNOS attenuates acute lung injury induced by

  17. Chronic obstructive pulmonary disease and obstructive sleep apnea: overlaps in pathophysiology, systemic inflammation, and cardiovascular disease.

    McNicholas, Walter T

    2012-02-01

    Chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea syndrome represent two of the most prevalent chronic respiratory disorders in clinical practice, and cardiovascular diseases represent a major comorbidity in each disorder. The two disorders coexist (overlap syndrome) in approximately 1% of adults but asymptomatic lower airway obstruction together with sleep-disordered breathing is more prevalent. Although obstructive sleep apnea syndrome has similar prevalence in COPD as the general population, and vice versa, factors such as body mass index and smoking influence relationships. Nocturnal oxygen desaturation develops in COPD, independent of apnea\\/hypopnea, and is more severe in the overlap syndrome, thus predisposing to pulmonary hypertension. Furthermore, upper airway flow limitation contributes to nocturnal desaturation in COPD without apnea\\/hypopnea. Evidence of systemic inflammation in COPD and sleep apnea, involving C-reactive protein and IL-6, in addition to nuclear factor-kappaB-dependent pathways involving tumor necrosis factor-alpha and IL-8, provides insight into potential basic interactions between both disorders. Furthermore, oxidative stress develops in each disorder, in addition to activation and\\/or dysfunction of circulating leukocytes. These findings are clinically relevant because systemic inflammation may contribute to the pathogenesis of cardiovascular diseases and the cell\\/molecular pathways involved are similar to those identified in COPD and sleep apnea. However, the pathophysiological and clinical significance of systemic inflammation in COPD and sleep apnea is not proven, and thus, studies of patients with the overlap syndrome should provide insight into the mechanisms of systemic inflammation in COPD and sleep apnea, in addition to potential relationships with cardiovascular disease.

  18. Eosinophilic airway inflammation: role in asthma and chronic obstructive pulmonary disease.

    George, Leena; Brightling, Christopher E

    2016-01-01

    The chronic lung diseases, asthma and chronic obstructive pulmonary disease (COPD), are common affecting over 500 million people worldwide and causing substantial morbidity and mortality. Asthma is typically associated with Th2-mediated eosinophilic airway inflammation, in contrast to neutrophilic inflammation observed commonly in COPD. However, there is increasing evidence that the eosinophil might play an important role in 10-40% of patients with COPD. Consistently in both asthma and COPD a sputum eosinophilia is associated with a good response to corticosteroid therapy and tailored strategies aimed to normalize sputum eosinophils reduce exacerbation frequency and severity. Advances in our understanding of the multistep paradigm of eosinophil recruitment to the airway, and the consequence of eosinophilic inflammation, has led to the development of new therapies to target these molecular pathways. In this article we discuss the mechanisms of eosinophilic trafficking, the tools to assess eosinophilic airway inflammation in asthma and COPD during stable disease and exacerbations and review current and novel anti-eosinophilic treatments. PMID:26770668

  19. Trace Levels of Staphylococcal Enterotoxin Bioactivity Are Concealed in a Mucosal Niche during Pulmonary Inflammation.

    Antoine Ménoret

    Full Text Available Pathogen and cellular by-products released during infection or trauma are critical for initiating mucosal inflammation. The localization of these factors, their bioactivity and natural countermeasures remain unclear. This concept was studied in mice undergoing pulmonary inflammation after Staphylococcal enterotoxin A (SEA inhalation. Highly purified bronchoalveolar lavage fluid (BALF fractions obtained by sequential chromatography were screened for bioactivity and subjected to mass spectrometry. The Inflammatory and inhibitory potentials of the identified proteins were measured using T cells assays. A potent pro-inflammatory factor was detected in BALF, and we hypothesized SEA could be recovered with its biological activity. Highly purified BALF fractions with bioactivity were subjected to mass spectrometry. SEA was the only identified protein with known inflammatory potential, and unexpectedly, it co-purified with immunosuppressive proteins. Among them was lactoferrin, which inhibited SEA and anti-CD3/-CD28 stimulation by promoting T cell death and reducing TNF synthesis. Higher doses of lactoferrin were required to inhibit effector compared to resting T cells. Inhibition relied on the continual presence of lactoferrin rather than a programming event. The data show a fraction of bioactive SEA resided in a mucosal niche within BALF even after the initiation of inflammation. These results may have clinical value in human diagnostic since traces levels of SEA can be detected using a sensitive bioassay, and may help pinpoint potential mediators of lung inflammation when molecular approaches fail.

  20. Spred-2 Deficiency Exacerbates Lipopolysaccharide-Induced Acute Lung Inflammation in Mice

    Yang Xu; Toshihiro Ito; Soichiro Fushimi; Sakuma Takahashi; Junya Itakura; Ryojiro Kimura; Miwa Sato; Megumi Mino; Akihiko Yoshimura; Akihiro Matsukawa

    2014-01-01

    BACKGROUND: Acute respiratory distress syndrome (ARDS) is a severe and life-threatening acute lung injury (ALI) that is caused by noxious stimuli and pathogens. ALI is characterized by marked acute inflammation with elevated alveolar cytokine levels. Mitogen-activated protein kinase (MAPK) pathways are involved in cytokine production, but the mechanisms that regulate these pathways remain poorly characterized. Here, we focused on the role of Sprouty-related EVH1-domain-containing protein (Spr...

  1. Inflammation of vertebral bone associated with acute calcific tendinitis of the longus colli muscle

    Mihmanli, I.; Kanberoglu, K. [Dept. of Radiology, Istanbul Univ. (Turkey); Karaarslan, E. [Intermed Medical Center, Nisantasi, Istanbul (Turkey)

    2001-12-01

    We present a case of acute retropharyngeal calcific tendinitis with characteristic findings on radiographic, computed tomography, and magnetic resonance imaging (MRI). To our knowledge, this is the first acute retropharyngeal calcific tendinitis report having inflammation of both the vertebra itself and the longus colli muscle diagnosed on MRI. In patients with neck pain, acute retropharyngeal calcific tendinitis should be kept in mind in the differential diagnosis, even if these patients had vertebral pathological signals on MRI. (orig.)

  2. Inflammation of vertebral bone associated with acute calcific tendinitis of the longus colli muscle

    We present a case of acute retropharyngeal calcific tendinitis with characteristic findings on radiographic, computed tomography, and magnetic resonance imaging (MRI). To our knowledge, this is the first acute retropharyngeal calcific tendinitis report having inflammation of both the vertebra itself and the longus colli muscle diagnosed on MRI. In patients with neck pain, acute retropharyngeal calcific tendinitis should be kept in mind in the differential diagnosis, even if these patients had vertebral pathological signals on MRI. (orig.)

  3. An Immature Myeloid/Myeloid-Suppressor Cell Response Associated with Necrotizing Inflammation Mediates Lethal Pulmonary Tularemia.

    Periasamy, Sivakumar; Avram, Dorina; McCabe, Amanda; MacNamara, Katherine C; Sellati, Timothy J; Harton, Jonathan A

    2016-03-01

    Inhalation of Francisella tularensis (Ft) causes acute and fatal pneumonia. The lung cytokine milieu favors exponential Ft replication, but the mechanisms underlying acute pathogenesis and death remain unknown. Evaluation of the sequential and systemic host immune response in pulmonary tularemia reveals that in contrast to overwhelming bacterial burden or cytokine production, an overt innate cellular response to Ft drives tissue pathology and host mortality. Lethal infection with Ft elicits medullary and extra-medullary myelopoiesis supporting recruitment of large numbers of immature myeloid cells and MDSC to the lungs. These cells fail to mature and die, leading to subsequent necrotic lung damage, loss of pulmonary function, and host death that is partially dependent upon immature Ly6G+ cells. Acceleration of this process may account for the rapid lethality seen with Ft SchuS4. In contrast, during sub-lethal infection with Ft LVS the pulmonary cellular response is characterized by a predominance of mature neutrophils and monocytes required for protection, suggesting a required threshold for lethal bacterial infection. Further, eliciting a mature phagocyte response provides transient, but dramatic, innate protection against Ft SchuS4. This study reveals that the nature of the myeloid cell response may be the primary determinant of host mortality versus survival following Francisella infection. PMID:27015566

  4. An Immature Myeloid/Myeloid-Suppressor Cell Response Associated with Necrotizing Inflammation Mediates Lethal Pulmonary Tularemia.

    Sivakumar Periasamy

    2016-03-01

    Full Text Available Inhalation of Francisella tularensis (Ft causes acute and fatal pneumonia. The lung cytokine milieu favors exponential Ft replication, but the mechanisms underlying acute pathogenesis and death remain unknown. Evaluation of the sequential and systemic host immune response in pulmonary tularemia reveals that in contrast to overwhelming bacterial burden or cytokine production, an overt innate cellular response to Ft drives tissue pathology and host mortality. Lethal infection with Ft elicits medullary and extra-medullary myelopoiesis supporting recruitment of large numbers of immature myeloid cells and MDSC to the lungs. These cells fail to mature and die, leading to subsequent necrotic lung damage, loss of pulmonary function, and host death that is partially dependent upon immature Ly6G+ cells. Acceleration of this process may account for the rapid lethality seen with Ft SchuS4. In contrast, during sub-lethal infection with Ft LVS the pulmonary cellular response is characterized by a predominance of mature neutrophils and monocytes required for protection, suggesting a required threshold for lethal bacterial infection. Further, eliciting a mature phagocyte response provides transient, but dramatic, innate protection against Ft SchuS4. This study reveals that the nature of the myeloid cell response may be the primary determinant of host mortality versus survival following Francisella infection.

  5. TLR4 signalling in pulmonary stromal cells is critical for inflammation and immunity in the airways

    Lambrecht Bart N

    2011-09-01

    Full Text Available Abstract Inflammation of the airways, which is often associated with life-threatening infection by Gram-negative bacteria or presence of endotoxin in the bioaerosol, is still a major cause of severe airway diseases. Moreover, inhaled endotoxin may play an important role in the development and progression of airway inflammation in asthma. Pathologic changes induced by endotoxin inhalation include bronchospasm, airflow obstruction, recruitment of inflammatory cells, injury of the alveolar epithelium, and disruption of pulmonary capillary integrity leading to protein rich fluid leak in the alveolar space. Mammalian Toll-like receptors (TLRs are important signalling receptors in innate host defense. Among these receptors, TLR4 plays a critical role in the response to endotoxin. Lungs are a complex compartmentalized organ with separate barriers, namely the alveolar-capillary barrier, the microvascular endothelium, and the alveolar epithelium. An emerging theme in the field of lung immunology is that structural cells (SCs of the airways such as epithelial cells (ECs, endothelial cells, fibroblasts and other stromal cells produce activating cytokines that determine the quantity and quality of the lung immune response. This review focuses on the role of TLR4 in the innate and adaptive immune functions of the pulmonary SCs.

  6. Immune modulatory effects of IL-22 on allergen-induced pulmonary inflammation.

    Ping Fang

    Full Text Available IL-22 is a Th17/Th22 cytokine that is increased in asthma. However, recent animal studies showed controversial findings in the effects of IL-22 in allergic asthma. To determine the role of IL-22 in ovalbumin-induced allergic inflammation we generated inducible lung-specific IL-22 transgenic mice. Transgenic IL-22 expression and signaling activity in the lung were determined. Ovalbumin (OVA-induced pulmonary inflammation, immune responses, and airway hyperresponsiveness (AHR were examined and compared between IL-22 transgenic mice and wild type controls. Following doxycycline (Dox induction, IL-22 protein was readily detected in the large (CC10 promoter and small (SPC promoter airway epithelial cells. IL-22 signaling was evidenced by phosphorylated STAT3. After OVA sensitization and challenge, compared to wild type littermates, IL-22 transgenic mice showed decreased eosinophils in the bronchoalveolar lavage (BAL, and in lung tissue, decreased mucus metaplasia in the airways, and reduced AHR. Among the cytokines and chemokines examined, IL-13 levels were reduced in the BAL fluid as well as in lymphocytes from local draining lymph nodes of IL-22 transgenic mice. No effect was seen on the levels of serum total or OVA-specific IgE or IgG. These findings indicate that IL-22 has immune modulatory effects on pulmonary inflammatory responses in allergen-induced asthma.

  7. Role of acid-sensing ion channel 3 in sub-acute-phase inflammation

    Chen Chien-Ju

    2009-01-01

    Full Text Available Abstract Background Inflammation-mediated hyperalgesia involves tissue acidosis and sensitization of nociceptors. Many studies have reported increased expression of acid-sensing ion channel 3 (ASIC3 in inflammation and enhanced ASIC3 channel activity with pro-inflammatory mediators. However, the role of ASIC3 in inflammation remains inconclusive because of conflicting results generated from studies of ASIC3 knockout (ASIC3-/- or dominant-negative mutant mice, which have shown normal, decreased or increased hyperalgesia during inflammation. Results Here, we tested whether ASIC3 plays an important role in inflammation of subcutaneous tissue of paw and muscle in ASIC3-/- mice induced by complete Freund's adjuvant (CFA or carrageenan by investigating behavioral and pathological responses, as well as the expression profile of ion channels. Compared with the ASIC3+/+ controls, ASIC3-/- mice showed normal thermal and mechanical hyperalgesia with acute (4-h intraplantar CFA- or carrageenan-induced inflammation, but the hyperalgesic effects in the sub-acute phase (1–2 days were milder in all paradigms except for thermal hyperalgesia with CFA-induced inflammation. Interestingly, carrageenan-induced primary hyperalgesia was accompanied by an ASIC3-dependent Nav1.9 up-regulation and increase of tetrodotoxin (TTX-resistant sodium currents. CFA-inflamed muscle did not evoke hyperalgesia in ASIC3-/- or ASIC3+/+ mice, whereas carrageenan-induced inflammation in muscle abolished mechanical hyperalgesia in ASIC3-/- mice, as previously described. However, ASIC3-/- mice showed attenuated pathological features such as less CFA-induced granulomas and milder carrageenan-evoked vasculitis as compared with ASIC3+/+ mice. Conclusion We provide a novel finding that ASIC3 participates in the maintenance of sub-acute-phase primary hyperalgesia in subcutaneous inflammation and mediates the process of granuloma formation and vasculitis in intramuscular inflammation.

  8. Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease

    Brill SE

    2014-11-01

    Full Text Available Simon E Brill, Jadwiga A Wedzicha Airway Disease Section, National Heart and Lung Institute, Imperial College, London, UK Abstract: Acute exacerbations of chronic obstructive pulmonary disease (COPD are important events in the history of this debilitating lung condition. Associated health care utilization and morbidity are high, and many patients require supplemental oxygen or ventilatory support. The last 2 decades have seen a substantial increase in our understanding of the best way to manage the respiratory failure suffered by many patients during this high-risk period. This review article examines the evidence underlying supplemental oxygen therapy during exacerbations of COPD. We first discuss the epidemiology and pathophysiology of respiratory failure in COPD during exacerbations. The rationale and evidence underlying oxygen therapy, including the risks when administered inappropriately, are then discussed, along with further strategies for ventilatory support. We also review current recommendations for best practice, including methods for improving oxygen provision in the future. Keywords: chronic obstructive pulmonary disease (COPD, exacerbation, oxygen therapy, respiratory failure, hypercapnia

  9. Hemoglobin-induced lung vascular oxidation, inflammation, and remodeling contribute to the progression of hypoxic pulmonary hypertension and is attenuated in rats with repeated-dose haptoglobin administration.

    Irwin, David C; Baek, Jin Hyen; Hassell, Kathryn; Nuss, Rachelle; Eigenberger, Paul; Lisk, Christina; Loomis, Zoe; Maltzahn, Joanne; Stenmark, Kurt R; Nozik-Grayck, Eva; Buehler, Paul W

    2015-05-01

    Haptoglobin (Hp) is an approved treatment in Japan for trauma, burns, and massive transfusion-related hemolysis. Additional case reports suggest uses in other acute hemolytic events that lead to acute kidney injury. However, Hp's protective effects on the pulmonary vasculature have not been evaluated within the context of mitigating the consequences of chronic hemoglobin (Hb) exposure in the progression of pulmonary hypertension (PH) secondary to hemolytic diseases. This study was performed to assess the utility of chronic Hp therapy in a preclinical model of Hb and hypoxia-mediated PH. Rats were simultaneously exposed to chronic Hb infusion (35 mg per day) and hypobaric hypoxia for 5 weeks in the presence or absence of Hp treatment (90 mg/kg twice a week). Hp inhibited the Hb plus hypoxia-mediated nonheme iron accumulation in lung and heart tissue, pulmonary vascular inflammation and resistance, and right-ventricular hypertrophy, which suggests a positive impact on impeding the progression of PH. In addition, Hp therapy was associated with a reduction in critical mediators of PH, including lung adventitial macrophage population and endothelial ICAM-1 expression. By preventing Hb-mediated pathology, Hp infusions: (1) demonstrate a critical role for Hb in vascular remodeling associated with hypoxia and (2) suggest a novel therapy for chronic hemolysis-associated PH. PMID:25656991

  10. Role of PGC-1α in acute and low-grade inflammation

    Olesen, Jesper

    The aim of the present thesis was to examine the role of the exercise-induced transcriptional co-activator, PGC-1α, in acute and low-grade inflammation. To investigate this, the following three hypotheses were tested: 1) Skeletal muscle PGC-1α plays an important role in acute LPS-induced systemic...... inflammation as well as in the inflammatory response in mouse skeletal muscle. 2) Long-term exercise training and/or resveratrol supplementation prevents age-associated low-grade- and skeletal muscle inflammation in mice with PGC-1α being required for these improvements. 3) Exercise training and/or resveratrol...... upplementation reduces systemic- as well as skeletal muscle inflammation in aged human subjects. Study I demonstrated an impaired LPS-induced plasma TNFα and skeletal muscle TNFα response in PGC-1α muscle specific knockout mice compared with WT mice. Conversely, mice with transgenic overexpression of PGC-1α in...

  11. Acute pulmonary emphysema cum pulmonary edema apparently associated with feeding of Brassica juncea in a dairy buffalo

    Muhammad, Ghulam; Saqib, Muhammad; NAUREEN, Abeera

    2010-01-01

    This preliminary report describes the occurrence of acute pulmonary emphysema cum pulmonary edema ensuing in extensive subcutaneous emphysematous swellings in a dairy buffalo (Bubalus bubalis) apparently associated with a sudden shift from berseem (Trifolium alexendrinum) to Brassica juncea fodder. Tachypnea, expiratory dyspnea, open-mouth breathing, loud expiratory grunt with abdominal lift, and crackles in ventral aspects of the lungs with normal rectal temperature characterized the conditi...

  12. Comparison Between the Acute Pulmonary Vascular Effects of Oxygen with Nitric Oxide and Sildenafil

    Ronald W. Day

    2015-03-01

    Full Text Available Objective. Right heart catheterization is performed in patients with pulmonary arterial hypertension to determine the severity of disease and their pulmonary vascular reactivity. The acute pulmonary vascular effect of inhaled nitric oxide is frequently used to identify patients who will respond favorably to vasodilator therapy. This study sought to determine whether the acute pulmonary vascular effects of oxygen with nitric oxide and intravenous sildenafil are similar. Methods. A retrospective, descriptive study of 13 individuals with pulmonary hypertension who underwent heart catheterization and acute vasodilator testing was performed. The hemodynamic measurements during five phases (21% to 53% oxygen, 100% oxygen, 100% oxygen with 20 ppm nitric oxide, 21% to 51% oxygen, and 21% to 51% oxygen with 0.05 mg/kg to 0.29 mg/kg intravenous sildenafil of the procedures were compared.Results. Mean pulmonary arterial pressure and pulmonary vascular resistance acutely decreased with 100% oxygen with nitric oxide, and 21% to 51% oxygen with sildenafil. Mean pulmonary arterial pressure (mm Hg, mean ± standard error of the mean was 38 ± 4 during 21% to 53% oxygen, 32 ± 3 during 100% oxygen, 29 ± 2 during 100% oxygen with nitric oxide, 37 ± 3 during 21% to 51% oxygen, and 32 ± 2 during 21% to 51% oxygen with sildenafil. There was not a significant correlation between the percent change in pulmonary vascular resistance from baseline with oxygen and nitric oxide, and from baseline with sildenafil (r2 = 0.011, p = 0.738. Conclusions. Oxygen with nitric oxide and sildenafil decreased pulmonary vascular resistance. However, the pulmonary vascular effects of oxygen and nitric oxide cannot be used to predict the acute response to sildenafil. Additional studies are needed to determine whether the acute response to sildenafil can be used to predict the long-term response to treatment with an oral phosphodiesterase V inhibitor.

  13. Anticoagulant treatment for acute pulmonary embolism: a pathophysiology-based clinical approach.

    Agnelli, Giancarlo; Becattini, Cecilia

    2015-04-01

    The management of patients with acute pulmonary embolism is made challenging by its wide spectrum of clinical presentation and outcome, which is mainly related to patient haemodynamic status and right ventricular overload. Mechanical embolic obstruction and neurohumorally mediated pulmonary vasoconstriction are responsible for right ventricular overload. The pathophysiology of acute pulmonary embolism is the basis for risk stratification of patients as being at high, intermediate and low risk of adverse outcomes. This risk stratification has been advocated to tailor clinical management according to the severity of pulmonary embolism. Anticoagulation is the mainstay of the treatment of acute pulmonary embolism. New direct oral anticoagulants, which are easier to use than conventional anticoagulants, have been compared with conventional anticoagulation in five randomised clinical trials including >11 000 patients with pulmonary embolism. Patients at high risk of pulmonary embolism (those with haemodynamic compromise) were excluded from these studies. Direct oral anticoagulants have been shown to be as effective and at least as safe as conventional anticoagulation in patients with pulmonary embolism without haemodynamic compromise, who are the majority of patients with this disease. Whether these agents are appropriate for the acute-phase treatment of patients at intermediate-high risk pulmonary embolism (those with both right ventricle dysfunction and injury) regardless of any risk stratification remains undefined. PMID:25700388

  14. Milano summer particulate matter (PM10 triggers lung inflammation and extra pulmonary adverse events in mice.

    Francesca Farina

    Full Text Available Recent studies have suggested a link between particulate matter (PM exposure and increased mortality and morbidity associated with pulmonary and cardiovascular diseases; accumulating evidences point to a new role for air pollution in CNS diseases. The purpose of our study is to investigate PM10sum effects on lungs and extra pulmonary tissues. Milano PM10sum has been intratracheally instilled into BALB/c mice. Broncho Alveolar Lavage fluid, lung parenchyma, heart and brain were screened for markers of inflammation (cell counts, cytokines, ET-1, HO-1, MPO, iNOS, cytotoxicity (LDH, ALP, Hsp70, Caspase8-p18, Caspase3-p17 for a putative pro-carcinogenic marker (Cyp1B1 and for TLR4 pathway activation. Brain was also investigated for CD68, TNF-α, GFAP. In blood, cell counts were performed while plasma was screened for endothelial activation (sP-selectin, ET-1 and for inflammation markers (TNF-α, MIP-2, IL-1β, MPO. Genes up-regulation (HMOX1, Cyp1B1, IL-1β, MIP-2, MPO and miR-21 have been investigated in lungs and blood. Inflammation in the respiratory tract of PM10sum-treated mice has been confirmed in BALf and lung parenchyma by increased PMNs percentage, increased ET-1, MPO and cytokines levels. A systemic spreading of lung inflammation in PM10sum-treated mice has been related to the increased blood total cell count and neutrophils percentage, as well as to increased blood MPO. The blood-endothelium interface activation has been confirmed by significant increases of plasma ET-1 and sP-selectin. Furthermore PM10sum induced heart endothelial activation and PAHs metabolism, proved by increased ET-1 and Cyp1B1 levels. Moreover, PM10sum causes an increase in brain HO-1 and ET-1. These results state the translocation of inflammation mediators, ultrafine particles, LPS, metals associated to PM10sum, from lungs to bloodstream, thus triggering a systemic reaction, mainly involving heart and brain. Our results provided additional insight into the toxicity

  15. Airway epithelial SPDEF integrates goblet cell differentiation and pulmonary Th2 inflammation.

    Rajavelu, Priya; Chen, Gang; Xu, Yan; Kitzmiller, Joseph A; Korfhagen, Thomas R; Whitsett, Jeffrey A

    2015-05-01

    Epithelial cells that line the conducting airways provide the initial barrier and innate immune responses to the abundant particles, microbes, and allergens that are inhaled throughout life. The transcription factors SPDEF and FOXA3 are both selectively expressed in epithelial cells lining the conducting airways, where they regulate goblet cell differentiation and mucus production. Moreover, these transcription factors are upregulated in chronic lung disorders, including asthma. Here, we show that expression of SPDEF or FOXA3 in airway epithelial cells in neonatal mice caused goblet cell differentiation, spontaneous eosinophilic inflammation, and airway hyperresponsiveness to methacholine. SPDEF expression promoted DC recruitment and activation in association with induction of Il33, Csf2, thymic stromal lymphopoietin (Tslp), and Ccl20 transcripts. Increased Il4, Il13, Ccl17, and Il25 expression was accompanied by recruitment of Th2 lymphocytes, group 2 innate lymphoid cells, and eosinophils to the lung. SPDEF was required for goblet cell differentiation and pulmonary Th2 inflammation in response to house dust mite (HDM) extract, as both were decreased in neonatal and adult Spdef(-/-) mice compared with control animals. Together, our results indicate that SPDEF causes goblet cell differentiation and Th2 inflammation during postnatal development and is required for goblet cell metaplasia and normal Th2 inflammatory responses to HDM aeroallergen. PMID:25866971

  16. Crosstalk between Inflammation and Coagulation in Acute Pancreatitis - Experimental and Clinical Studies.

    Andersson, Ellen

    2010-01-01

    In various inflammatory conditions a close interplay between inflammation and coagulation is known to exist, where coagulation factor VII (FVII) and tissue factor (TF) are considered to be pivotal players. In this thesis the crosstalk between inflammation and coagulation in acute pancreatitis (AP) has been investigated. The results from the first paper, where active site inactivated FVII (FVIIai) is given as pre-treatment in a rat model of severe AP, show a decreased inflammatory respo...

  17. Novel Lipid Mediators and Resolution Mechanisms in Acute Inflammation: To Resolve or Not?

    Serhan, Charles N.

    2010-01-01

    Because inflammation is appreciated as a unifying basis of many widely occurring diseases, the mechanisms involved in its natural resolution are of considerable interest. Using contained, self-limited inflammatory exudates and a systems approach, novel lipid-derived mediators and pathways were uncovered in the resolution of inflammatory exudates. These new families of local mediators control both the duration and magnitude of acute inflammation as well as the return of the site to homeostasis...

  18. Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation.

    Johnson, Ariel M; Kurti, Stephanie P; Smith, Joshua R; Rosenkranz, Sara K; Harms, Craig A

    2016-03-01

    A high-fat meal (HFM) induces an increase in blood lipids (postprandial lipemia; PPL), systemic inflammation, and acute airway inflammation. While acute exercise has been shown to have anti-inflammatory and lipid-lowering effects, it is unknown whether exercise prior to an HFM will translate to reduced airway inflammation post-HFM. Our purpose was to determine the effects of an acute bout of exercise on airway inflammation post-HFM and to identify whether any protective effect of exercise on airway inflammation was associated with a reduction in PPL or systemic inflammation. In a randomized cross-over study, 12 healthy, 18- to 29-year-old men (age, 23.0 ± 3.2 years; height, 178.9 ± 5.5 cm; weight, 78.5 ± 11.7 kg) consumed an HFM (1 g fat/1 kg body weight) 12 h following exercise (EX; 60 min at 60% maximal oxygen uptake) or without exercise (CON). Fractional exhaled nitric oxide (FENO; measure of airway inflammation), triglycerides (TG), and inflammatory markers (high-sensitivity C-reactive protein, tumor-necrosis factor-alpha, and interleukin-6) were measured while fasted at 2 h and 4 h post-HFM. FENO increased over time (2 h: CON, p = 0.001; EX, p = 0.002, but not by condition (p = 0.991). TG significantly increased 2 and 4 h post-HFM (p 0.05). There were no relationships between FENO and TG or systemic inflammatory markers for any time point or condition (p > 0.05). In summary, an acute bout of moderate-intensity exercise performed 12 h prior to an HFM did not change postprandial airway inflammation or lipemia in healthy, 18- to 29-year-old men. PMID:26872295

  19. Pulmonary Thromboembolism Complicating Acute Pancreatitis With Pancreatic Ascites: A Series of 4 cases

    Ruchir Patel

    2016-05-01

    Full Text Available Acute pancreatitis is an inflammatory disease often associated with local and systemic complications. Portosplenic and splanchnic vascular complications of acute pancreatitis are common, but extrasplanchnic vessel thrombosis is less commonly seen. Among them, pulmonary thromboembolism is a very rare complication to be encountered with. We report four cases of acute pulmonary thromboembolism in patients with acute pancreatitis superimposed on chronic pancreatitis. All the patients had abdominal pain on presentation and distention of abdomen during the course. Dyspnea was present in all the patients. All patients were found to have pancreatic ascites, whose association with pulmonary thromboembolism is reported only in two patients till date upto our knowledge. Two of them had deep vein thrombosis and rest two had no venous thrombosis. All of them were managed conservatively using subcutaneous heparin, intravenous fluids and analgesics. We provide the causative mechanism for occurrence of pulmonary thromboembolism in acute on chronic pancreatitis. We have also hypothesized pancreatic ascites as the possible cause for pulmonary thromboembolism and provide explanation for it. We conclude that pulmonary thromboembolism in acute pancreatitis has good prognosis if diagnosed timely. Whenever patient with pancreatic ascites presents with dyspnea, pulmonary thromboembolism must be ruled out.

  20. Correlates of syncope in patients with acute pulmonary thromboembolism.

    Jenab, Yaser; Lotfi-Tokaldany, Masoumeh; Alemzadeh-Ansari, Mohammad-Javad; Seyyedi, Seyyed Reza; Shirani, Shapoor; Soudaee, Mehdi; Ghaffari-Marandi, Neda

    2015-11-01

    Identification of pulmonary thromboembolism (PTE), as a cause of syncope, is important and may be life saving. We prospectively analyzed data on 335 patients with acute PTE. Relationships between syncope secondary to acute PTE and clinical findings, risk factors, and imaging modalities were analyzed. Of the 335 patients, 36 (10.7%) had syncope at presentation. Compared to patients without syncope, those with syncope had a higher frequency of right ventricular (RV) dysfunction (94.3% vs 72.1%, respectively; P value = .004) and saddle embolism (24.2% vs 10.9%, respectively; P value = .044). Frequency of RV dysfunction was similar between patients with and without saddle embolism. Although not significant, more patients with syncope had a history of previous PTE (P value = .086). By multivariable analysis, RV dysfunction and saddle embolism were independent correlates of syncope in patients with PTE. In-hospital mortality was not significantly different between the groups. In conclusion, among patients with PTE, RV dysfunction and saddle embolism were the independent correlates of syncope. PMID:24989710

  1. HRCT in AIDS patients presenting with acute pulmonary conditions

    Purpose: The purpose of this study was to assess the clinical value of HRCT of the lung in patients with known HIV-infection and acute lung disease. In a prospective study a HRCT was performed in 31 patients infected with the HIV-1 virus, mainly stage C (CDC), who had acute pulmonary symptoms. Precondition for the HRCT examination was a normal or non-specific chest radiograph. A provoked sputum as well as bronchoscopy with bronchoalveolar lavage and/or transbronchial biopsy were performed concurrently. In 24 out of 31 cases a pathogenic organism was identified. 19 of these 24 patients showed abnormal HRCT findings. The most frequent pathogenic organism was Pneumocystis carinii (n=12). 9 out of these 12 patients (75%) showed pathological HRCT findings consisting of ground-glass opacity. Specific patterns of attenuation could not be worked out except for Pneumocystis carinii infection. Compared to bronchoalveolar lavage, the diagnostic value of HRCT is inferior; it is however helpful in the early stage of disease, when the pathogenic organism has not yet been identified, HRCT may demonstrate parenchymal abnormalities in patients with normal radiographic findings. Compared to bronchoalveolar lavage and induced sputum, HRCT can provide conclusive results within a short time. (orig.)

  2. Gas exchange and pulmonary hypertension following acute pulmonary thromboembolism: has the emperor got some new clothes yet?

    Tsang, John Y C; Hogg, James C

    2014-06-01

    Patients present with a wide range of hypoxemia after acute pulmonary thromboembolism (APTE). Recent studies using fluorescent microspheres demonstrated that the scattering of regional blood flows after APTE, created by the embolic obstruction unique in each patient, significantly worsened regional ventilation/perfusion (V/Q) heterogeneity and explained the variability in gas exchange. Furthermore, earlier investigators suggested the roles of released vasoactive mediators in affecting pulmonary hypertension after APTE, but their quantification remained challenging. The latest study reported that mechanical obstruction by clots accounted for most of the increase in pulmonary vascular resistance, but that endothelin-mediated vasoconstriction also persisted at significant level during the early phase. PMID:25006441

  3. Effects of vagus nerve stimulation and vagotomy on systemic and pulmonary inflammation in a two-hit model in rats.

    Matthijs Kox

    Full Text Available Pulmonary inflammation contributes to ventilator-induced lung injury. Sepsis-induced pulmonary inflammation (first hit may be potentiated by mechanical ventilation (MV, second hit. Electrical stimulation of the vagus nerve has been shown to attenuate inflammation in various animal models through the cholinergic anti-inflammatory pathway. We determined the effects of vagotomy (VGX and vagus nerve stimulation (VNS on systemic and pulmonary inflammation in a two-hit model. Male Sprague-Dawley rats were i.v. administered lipopolysaccharide (LPS and subsequently underwent VGX, VNS or a sham operation. 1 hour following LPS, MV with low (8 mL/kg or moderate (15 mL/kg tidal volumes was initiated, or animals were left breathing spontaneously (SP. After 4 hours of MV or SP, rats were sacrificed. Cytokine and blood gas analysis was performed. MV with 15, but not 8 mL/kg, potentiated the LPS-induced pulmonary pro-inflammatory cytokine response (TNF-α, IL-6, KC: p<0.05 compared to LPS-SP, but did not affect systemic inflammation or impair oxygenation. VGX enhanced the LPS-induced pulmonary, but not systemic pro-inflammatory cytokine response in spontaneously breathing, but not in MV animals (TNF-α, IL-6, KC: p<0.05 compared to SHAM, and resulted in decreased pO(2 (p<0.05 compared to sham-operated animals. VNS did not affect any of the studied parameters in both SP and MV animals. In conclusion, MV with moderate tidal volumes potentiates the pulmonary inflammatory response elicited by systemic LPS administration. No beneficial effects of vagus nerve stimulation performed following LPS administration were found. These results questions the clinical applicability of stimulation of the cholinergic anti-inflammatory pathway in systemically inflamed patients admitted to the ICU where MV is initiated.

  4. Invariant Natural Killer T (iNKT Cells Prevent Autoimmunity, but Induce Pulmonary Inflammation in Cystic Fibrosis

    Nanna Siegmann

    2014-06-01

    Full Text Available Background/Aims: Inflammation is a major and critical component of the lung pathology in the hereditary disease cystic fibrosis. The molecular mechanisms of chronic inflammation in cystic fibrosis require definition. Methods: We used several genetic mouse models to test a role of iNKT cells and ceramide in pulmonary inflammation of cystic fibrosis mice. Inflammation was determined by the pulmonary cytokine profil and the abundance of inflammatory cells in the lung. Results: Here we provide a new concept how inflammation in the lung of individuals with cystic fibrosis is initiated. We show that in cystic fibrosis mice the mutation in the Cftr gene provokes a significant up-regulation of iNKT cells in the lung. Accumulation of iNKT cells serves to control autoimmune disease, which is triggered by a ceramide-mediated induction of cell death in CF organs. Autoimmunity becomes in particular overt in cystic fibrosis mice lacking iNKT cells and although suppression of the autoimmune response by iNKT cells is beneficial, IL-17+ iNKT cells attract macrophages and neutrophils to CF lungs resulting in chronic inflammation. Genetic deletion of iNKT cells in cystic fibrosis mice prevents inflammation in CF lungs. Conclusion: Our data demonstrate an important function of iNKT cells in the chronic inflammation affecting cystic fibrosis lungs. iNKT cells suppress the auto-immune response induced by ceramide-mediated death of epithelial cells in CF lungs, but also induce a chronic pulmonary inflammation.

  5. Lung inflammation and genotoxicity following pulmonary exposure to nanoparticles in ApoE-/- mice

    Ladefoged Ole

    2009-01-01

    Full Text Available Abstract Background The toxic and inflammatory potential of 5 different types of nanoparticles were studied in a sensitive model for pulmonary effects in apolipoprotein E knockout mice (ApoE-/-. We studied the effects instillation or inhalation Printex 90 of carbon black (CB and compared CB instillation in ApoE-/- and C57 mice. Three and 24 h after pulmonary exposure, inflammation was assessed by mRNA levels of cytokines in lung tissue, cell composition, genotoxicity, protein and lactate dehydrogenase activity in broncho-alveolar lavage (BAL fluid. Results Firstly, we found that intratracheal instillation of CB caused far more pulmonary toxicity in ApoE-/- mice than in C57 mice. Secondly, we showed that instillation of CB was more toxic than inhalation of a presumed similar dose with respect to inflammation in the lungs of ApoE-/- mice. Thirdly, we compared effects of instillation in ApoE-/- mice of three carbonaceous particles; CB, fullerenes C60 (C60 and single walled carbon nanotubes (SWCNT as well as gold particles and quantum dots (QDs. Characterization of the instillation media revealed that all particles were delivered as agglomerates and aggregates. Significant increases in Il-6, Mip-2 and Mcp-1 mRNA were detected in lung tissue, 3 h and 24 h following instillation of SWCNT, CB and QDs. DNA damage in BAL cells, the fraction of neutrophils in BAL cells and protein in BAL fluid increased statistically significantly. Gold and C60 particles caused much weaker inflammatory responses. Conclusion Our data suggest that ApoE-/- model is sensitive for evaluating particle induced inflammation. Overall QDs had greatest effects followed by CB and SWCNT with C60 and gold being least inflammatory and DNA-damaging. However the gold was used at a much lower mass dose than the other particles. The strong effects of QDs were likely due to Cd release. The surface area of the instilled dose correlated well the inflammatory response for low toxicity particles.

  6. The Effect of PPE-Induced Emphysema and Chronic LPS-Induced Pulmonary Inflammation on Atherosclerosis Development in APOE*3-LEIDEN Mice

    Khedoe, P.P.S.J.; Wong, M C; Wagenaar, G.T.M.; Plomp, J. J.; Eck, M; Havekes, L. M.; Rensen, P.C.N.; Hiemstra, P. S.; Berbée, J.F.P.

    2013-01-01

    Background: Chronic obstructive pulmonary disease (COPD) is characterized by pulmonary inflammation, airways obstruction and emphysema, and is a risk factor for cardiovascular disease (CVD). However, the contribution of these individual COPD components to this increased risk is unknown. Therefore, the aim of this study was to determine the contribution of emphysema in the presence or absence of pulmonary inflammation to the increased risk of CVD, using a mouse model for atherosclerosis. Becau...

  7. Pulmonary embolism with acute pancreatitis: A case report and literature review

    Qing Zhang; Qing-Xia Zhang; Xiao-Ping Tan; Wei-Zheng Wang; Chang-Hua He; Li Xu; Xiao-Xia Huang

    2012-01-01

    Acute pancreatitis is an inflammatory disease characterized by local tissue injury which can trigger a systemic inflammatory response. So vascular complications of pancreatitis are a major cause of morbidity and mortality. Pulmonary embolism in acute pancreatitis has been reported to be very rare. We reported a case of pulmonary embolism with acute pancreatitis. A 38-year-old woman broke out upper abdomen pain without definite inducement. She had no nausea and vomiting, fever, dyspnea, cough and expectoration, chest pain. The patient had been diagnosed with acute pancreatitis in local hospital. The patient was treated with antibiotics and proton pump inhibitors, and the abdomen pain was alleviated slightly. But the patient came forth cough and expectoration with a little blood, progressive dyspnea. A computed tomographic scan of the abdomen revealed pancreatitis. Subsequent computer tomography angiography of chest revealed pulmonary embolism (both down pulmonary arteries, left pulmonary artery and branch of right pulmonary artery). Dyspnea of the patient got well with thrombolytic treatment and anti-coagulation therapy. Pulmonary embolism is a rare but potentially lethal complication of pancreatitis. Familiarity with this complication will aid in its early diagnosis, therapy and prevent pulmonary embolism, a rare but catastrophic phenomenon.

  8. Systemic Inflammation and Reperfusion Injury in Patients With Acute Myocardial Infarction

    Fien Blancke; Marc J. Claeys; Philippe Jorens; Guy Vermeiren; Johan Bosmans; Wuyts, Floris L; Vrints, Chris J.

    2005-01-01

    Despite early recanalization of an occluded infarct artery, tissue reperfusion remains impaired in more than one-third of the acute myocardial infarction (AMI) patients owing to a process of reperfusion injury. The role of systemic inflammation in triggering this phenomenon is unknown. Proinflammatory factors (hs-CRP, TNF-α) and anti-inflammatory mediators (IL-1 receptor antagonist, IL-10) were measured in 65 patients during the acute phase of a myocardial infarction as well as in 11 healthy ...

  9. Sildenafil versus nitric oxide for acute vasodilator testing in pulmonary arterial hypertension

    Milger, Katrin; Felix, Janine F.; Voswinckel, Robert; Sommer, Natascha; Franco, Oscar H; Grimminger, Friedrich; Reichenberger, Frank; Seeger, Werner; Ghofrani, Hossein A; Gall, Henning

    2015-01-01

    Vasoreactivity testing with inhaled NO is recommended for pulmonary arterial hypertension (PAH) because of its therapeutic and prognostic value. Sildenafil has acute pulmonary vasodilating properties, but its diagnostic and prognostic impact in PAH is unknown. Our objective was to compare acute vasodilating responses to sildenafil and those to NO during right heart catheterization and also their prognostic values in patients with PAH. Ninety-nine patients with idiopathic PAH and 99 with assoc...

  10. Nicardipine-Induced Acute Pulmonary Edema: A Rare but Severe Complication of Tocolysis

    Claire Serena; Emmanuelle Begot; Jérôme Cros; Charles Hodler; Anne Laure Fedou; Nathalie Nathan-Denizot; Marc Clavel

    2014-01-01

    We report four cases of acute pulmonary edema that occurred during treatment by intravenous tocolysis using nicardipine in pregnancy patients with no previous heart problems. Clinical severity justified hospitalization in intensive care unit (ICU) each time. Acute dyspnea has begun at an average of 63 hours after initiation of treatment. For all patients, the first diagnosis suspected was pulmonary embolism. The patients' condition improved rapidly with appropriate diuretic treatment and by m...

  11. Cross sectional Doppler echocardiography as the initial technique for the diagnosis of acute pulmonary embolism.

    Cheriex, E. C.; Sreeram, N.; Eussen, Y F; Pieters, F A; Wellens, H J

    1994-01-01

    OBJECTIVE--To determine the value of cross sectional Doppler echocardiography and derived indices of right ventricular pressure and function in the initial diagnosis of pulmonary embolism. BACKGROUND--Most deaths from acute pulmonary embolism occur because of a delay in diagnosis. Ventilation-perfusion scans are not sufficiently sensitive, whereas angiography is invasive and associated with complications. The use of cross sectional Doppler echocardiography to assess acute changes in right ven...

  12. Mast cell stabilization alleviates acute lung injury after orthotopic autologous liver transplantation in rats by downregulating inflammation.

    Ailan Zhang

    Full Text Available BACKGROUND: Acute lung injury (ALI is one of the most severe complications after orthotopic liver transplantation. Amplified inflammatory response after transplantation contributes to the process of ALI, but the mechanism underlying inflammation activation is not completely understood. We have demonstrated that mast cell stabilization attenuated inflammation and ALI in a rodent intestine ischemia/reperfusion model. We hypothesized that upregulation of inflammation triggered by mast cell activation may be involve in ALI after liver transplantation. METHODS: Adult male Sprague-Dawley rats received orthotopic autologous liver transplantation (OALT and were executed 4, 8, 16, and 24 h after OALT. The rats were pretreated with the mast cell stabilizers cromolyn sodium or ketotifen 15 min before OALT and executed 8 h after OALT. Lung tissues and arterial blood were collected to evaluate lung injury. β-hexosaminidase and mast cell tryptase levels were assessed to determine the activation of mast cells. Tumor necrosis factor α (TNF-α, interleukin (IL-1β and IL-6 in serum and lung tissue were analyzed by enzyme-linked immunosorbent assay. Nuclear factor-kappa B (NF-κB p65 translocation was assessed by Western blot. RESULTS: The rats that underwent OALT exhibited severe pulmonary damage with a high wet-to-dry ratio, low partial pressure of oxygen, and low precursor surfactant protein C levels, which corresponded to the significant elevation of pro-inflammatory cytokines, β-hexosaminidase, and tryptase levels in serum and lung tissues. The severity of ALI progressed and maximized 8 h after OALT. Mast cell stabilization significantly inhibited the activation of mast cells, downregulated pro-inflammatory cytokine levels and translocation of NF-κB, and attenuated OALT-induced ALI. CONCLUSIONS: Mast cell activation amplified inflammation and played an important role in the process of post-OALT related ALI.

  13. Acute exacerbations of chronic obstructive pulmonary disease: causes and impacts.

    Chhabra, Sunil K; Dash, Devi Jyoti

    2014-01-01

    Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are recognised clinically as episodes of increased breathlessness and productive cough requiring a more intensive treatment. A subset of patients with this disease is especially prone to such exacerbations. These patients are labelled as 'frequent exacerbators'. Though yet poorly characterised in terms of host characteristics, including any genetic basis, these patients are believed to represent a distinct phenotype as they have a different natural history with a more progressive disease and a poorer prognosis than those who get exacerbations infrequently. Most exacerbations appear to be associated with infective triggers, either bacterial or viral, although 'non-infective' agents, such as air pollution and other irritants may also be important. Susceptibility to exacerbations is determined by multiple factors. Several risk factors have been identified, some of which are modifiable. Chronic obstructive pulmonary disease (COPD) exacerbations are major drivers of health status and patient-centered outcomes, and are a major reason for health care utilisation including hospitalisations and intensive care admissions. These are associated with considerable morbidity and mortality, both immediate and long-term. These episodes have a negative impact on the patient and the disease including high economic burden, increased mortality, worsening of health status, limitation of activity, and aggravation of comorbidities including cardiovascular disease, osteoporosis and neuro-psychiatric complications. Exacerbations also increase the rate of progression of disease, increasing the annual decline in lung function and leading to a poorer prognosis. Evaluation of risk of exacerbations is now included as a major component of the initial assessment of a patient with COPD in addition to the traditionally used lung function parameter, forced expiratory volume in one second (FEV1). Decreasing the risk of exacerbations

  14. Clinical presentation of acute pulmonary embolism: survey of 800 cases.

    Massimo Miniati

    Full Text Available BACKGROUND: Pulmonary embolism (PE is a common and potentially fatal disease that is still underdiagnosed. The objective of our study was to reappraise the clinical presentation of PE with emphasis on the identification of the symptoms and signs that prompt the patients to seek medical attention. METHODOLOGY/PRINCIPAL FINDINGS: We studied 800 patients with PE from two different clinical settings: 440 were recruited in Pisa (Italy as part of the Prospective Investigative Study of Acute Pulmonary Embolism Diagnosis (PISAPED; 360 were diagnosed with and treated for PE in seven hospitals of central Tuscany, and evaluated at the Atherothrombotic Disorders Unit, Firenze (Italy, shortly after hospital discharge. We interviewed the patients directly using a standardized, self-administered questionnaire originally utilized in the PISAPED. The two samples differed significantly as regards age, proportion of outpatients, prevalence of unprovoked PE, and of active cancer. Sudden onset dyspnea was the most frequent symptom in both samples (81 and 78%, followed by chest pain (56 and 39%, fainting or syncope (26 and 22%, and hemoptysis (7 and 5%. At least one of the above symptoms was reported by 756 (94% of 800 patients. Isolated symptoms and signs of deep vein thrombosis occurred in 3% of the cases. Only 7 (1% of 800 patients had no symptoms before PE was diagnosed. CONCLUSIONS/SIGNIFICANCE: Most patients with PE feature at least one of four symptoms which, in decreasing order of frequency, are sudden onset dyspnea, chest pain, fainting (or syncope, and hemoptysis. The occurrence of such symptoms, if not explained otherwise, should alert the clinicians to consider PE in differential diagnosis, and order the appropriate objective test.

  15. A Quantitative Model of Thermal Injury-Induced Acute Inflammation

    Yang, Qian; Berthiaume, Francois; Androulakis, Ioannis P.

    2010-01-01

    Severe burns are among the most common causes of death from unintentional injury. The induction and resolution of the burn-induced systemic inflammatory response are mediated by a network of factors and regulatory proteins. Numerous mechanisms operate simultaneously, thus requiring a systems level approach to characterize their overall impact. Towards this goal, we propose an in silico semi-mechanistic model of burn-induced systemic inflammation using liver specific gene expression from a rat...

  16. Morphological changes in small pulmonary vessels are associated with severe acute exacerbation in chronic obstructive pulmonary disease

    Yoshimura K

    2016-06-01

    Full Text Available Katsuhiro Yoshimura,1,2 Yuzo Suzuki,1,2 Tomohiro Uto,2 Jun Sato,2 Shiro Imokawa,2 Takafumi Suda1 1Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan; 2Department of Respiratory Medicine, Iwata City Hospital, Iwata, Japan Background: Pulmonary vascular remodeling is essential for understanding the pathogenesis of chronic obstructive pulmonary disease (COPD. The total cross-sectional area (CSA of small pulmonary vessels has been reported to correlate with the pulmonary artery pressure, and this technique has enabled the assessment of pulmonary vascular involvements. We investigated the contribution of morphological alterations in the pulmonary vessels to severe acute exacerbation of COPD (AE-COPD.Methods: This study enrolled 81 patients with COPD and 28 non-COPD subjects as control and assessed the percentage of CSA (%CSA less than 5 mm2 (%CSA<5 and %CSA in the range of 5–10 mm2 (%CSA5–10 on high-resolution computed tomography images.Results: Compared with the non-COPD subjects, the COPD patients had lower %CSA<5. %CSA<5 was positively correlated with airflow limitation and negatively correlated with the extent of emphysema. COPD patients with lower %CSA<5 showed significantly increased incidences of severe AE-COPD (Gray’s test; P=0.011. Furthermore, lower %CSA<5 was significantly associated with severe AE-COPD (hazard ratio, 2.668; 95% confidence interval, 1.225–5.636; P=0.010.Conclusion: %CSA<5 was associated with an increased risk of severe AE-COPD. The distal pruning of the small pulmonary vessels is a part of the risk associated with AE-COPD, and %CSA<5 might be a surrogate marker for predicting AE-COPD. Keywords: chronic obstructive pulmonary disease (COPD, acute exacerbation, pulmonary vessels, cross-sectional area (CSA, computed tomography

  17. Pulmonary Artery Dilation and Right Ventricular Function in Acute Kawasaki Disease.

    Numano, Fujito; Shimizu, Chisato; Tremoulet, Adriana H; Dyar, Dan; Burns, Jane C; Printz, Beth F

    2016-03-01

    Coronary artery inflammation and aneurysm formation are the most common complications of Kawasaki disease (KD). Valvulitis and myocarditis are also well described and may lead to valvar regurgitation and left ventricular dysfunction. However, functional changes in the right heart have rarely been reported. We noted several acute KD patients with dilated pulmonary arteries (PA) and thus sought to systematically characterize PA size and right-heart function in an unselected cohort of KD patients cared for at a single clinical center. Clinical, laboratory, and echocardiographic data from 143 acute KD subjects were analyzed. PA dilation was documented in 23 subjects (16.1 %); these subjects had higher median right ventricle myocardial performance index (RV MPI), higher ratio of early tricuspid inflow velocity to tricuspid annular early diastolic velocity (TV E/e'), and lower median TV e' velocity compared to the non-PA dilation group (0.50 vs 0.38 p < 0.01, 4.2 vs 3.6 p < 0.05, and 13.5 vs 15.2 cm/s p < 0.01, respectively). Almost all subjects with PA dilation had improved PA Z-score, RV MPI, and TV E/e' in the subacute phase (p < 0.01). There were no significant differences in indices of left ventricle function between PA dilation group and non-PA dilation group. In summary, PA dilation was documented in 16 % of acute KD subjects. These subjects were more likely to have echocardiographic indices consistent with isolated RV dysfunction that improved in the subacute phase. The long-term consequence of these findings will require longitudinal studies of this patient population. PMID:26681305

  18. Erythropoietin augments the cytokine response to acute endotoxin-induced inflammation in humans

    Hojman, Pernille; Taudorf, Sarah; Lundby, Carsten;

    2009-01-01

    Recent studies have shown that erythropoietin (EPO) offers protection against ischemia, hemorrhagic shock and systemic inflammation in many tissues and it has been suggested that EPO has anti-inflammatory effects. With the aim of investigating the potential acute anti-inflammatory effects of EPO in...

  19. Macrophage activation in acute exacerbation of idiopathic pulmonary fibrosis.

    Jonas Christian Schupp

    Full Text Available Acute exacerbation (AE of idiopathic pulmonary fibrosis (IPF is a common cause of disease acceleration in IPF and has a major impact on mortality. The role of macrophage activation in AE of IPF has never been addressed before.We evaluated BAL cell cytokine profiles and BAL differential cell counts in 71 IPF patients w/wo AE and in 20 healthy volunteers. Twelve patients suffered from AE at initial diagnosis while sixteen patients developed AE in the 24 months of follow-up. The levels of IL-1ra, CCL2, CCL17, CCL18, CCL22, TNF-α, IL-1β, CXCL1 and IL-8 spontaneously produced by BAL-cells were analysed by ELISA.In patients with AE, the percentage of BAL neutrophils was significantly increased compared to stable patients. We found an increase in the production rate of the pro-inflammatory cytokines CXCL1 and IL-8 combined with an increase in all tested M2 cytokines by BAL-cells. An increase in CCL18 levels and neutrophil counts during AE was observed in BAL cells from patients from whom serial lavages were obtained. Furthermore, high baseline levels of CCL18 production by BAL cells were significantly predictive for the development of future AE.BAL cell cytokine production levels at acute exacerbation show up-regulation of pro-inflammatory as well as anti-inflammatory/ M2 cytokines. Our data suggest that AE in IPF is not an incidental event but rather driven by cellular mechanisms including M2 macrophage activation.

  20. Montelukast versus Dexamethasone Treatment in a Guinea Pig Model of Chronic Pulmonary Neutrophilic Inflammation.

    Abdel Kawy, Hala S

    2016-08-01

    Airway inflammation in chronic obstructive pulmonary disease (COPD) is refractory to corticosteroids and hence COPD treatment is hindered and insufficient. This study assessed the effects of oral treatment with Montelukast (10 and 30 mg/kg) or dexamethasone (20 mg/kg) for 20 days on COPD model induced by chronic exposure to lipopolysaccharide (LPS). Six groups of male guinea pigs were studied. Group 1: naïve group, group 2: exposed to saline nebulization. Groups 3, 4, 5, and 6: exposed to 9 nebulizations of LPS (30 μg/ml) for 1 hour, 48 hours apart with or without treatment with Montelukast or dexamethasone. Airway hyperreactivity (AHR) to methacholine (MCh), histopathological study and bronchoalveolar lavage fluid (BALF) as well as lung tissue analyses were performed 48 hours after the final exposure to LPS (day 20). LPS-induced pulmonary dysfunction was associated with increased neutrophil count, leukotriene (LT) B4, and tumor necrosis factor (TNF)-α in BALF. Moreover, there was an increase in malondialdehyde (MDA) level and a decrease in histone deacetylases(HDAC) activity in the lung tissue. Both Montelukast (10 or 30 mg /kg) and dexamethasone significantly reduced neutrophil count in BALF and inflammatory cells in lung parenchyma as well as TNF-α, and MDA levels. However, dexamethasone was more effective (p dexamethasone. These results suggest that treatment with Montelukast can be useful in chronic airway inflammatory diseases including COPD poorly responsive to glucocorticoids. PMID:26751767

  1. Pulmonary inflammation and crystalline silica in respirable coal mine dust: dose-response

    E D Kuempel; M D Attfield; V Vallyathan; N L Lapp; J M Hale; R J Smith; V Castranova

    2003-02-01

    This study describes the quantitative relationships between early pulmonary responses and the estimated lungburden or cumulative exposure of respirable-quartz or coal mine dust. Data from a previous bronchoalveolar lavage (BAL) study in coal miners ( = 20) and nonminers ( = 16) were used including cell counts of alveolar macrophages (AMs) and polymorphonuclear leukocytes (PMNs), and the antioxidant superoxide dismutase (SOD) levels. Miners’ individual working lifetime particulate exposures were estimated from work histories and mine air sampling data, and quartz lung-burdens were estimated using a lung dosimetry model. Results show that quartz, as either cumulative exposure or estimated lung-burden, was a highly statistically significant predictor of PMN response ( < 0.0001); however cumulative coal dust exposure did not significantly add to the prediction of PMNs ( = 0.2) above that predicted by cumulative quartz exposure ( < 0.0001). Despite the small study size, radiographic category was also significantly related to increasing levels of both PMNs and quartz lung burden (-values < 0.04). SOD in BAL fluid rose linearly with quartz lung burden ( < 0.01), but AM count in BAL fluid did not ( > 0.4). This study demonstrates dose-response relationships between respirable crystalline silica in coal mine dust and pulmonary inflammation, antioxidant production, and radiographic small opacities.

  2. The Prevalence of Oral Inflammation Among Denture Wearing Patients with Chronic Obstructive Pulmonary Disease.

    Przybyłowska, D; Rubinsztajn, R; Chazan, R; Swoboda-Kopeć, E; Kostrzewa-Janicka, J; Mierzwińska-Nastalska, E

    2015-01-01

    Oral inflammation is an important contributor to the etiology of chronic obstructive pulmonary disease, which can impact patient's health status. Previous studies indicate that people with poor oral health are at higher risk for nosocomial pneumonia. Denture wearing is one promoting factor in the development of mucosal infections. Colonization of the denture plaque by Gram-negative bacteria, Candida spp., or other respiratory pathogens, occurring locally, may be aspirated to the lungs. The studies showed that chronic obstructive pulmonary disease (COPD) patients treated with combinations of medicines with corticosteroids more frequently suffer from Candida-associated denture stomatitis. Treatment of oral candidiasis in patients with COPD constitutes a therapeutic problem. Therefore, it is essential to pay attention to the condition of oral mucosal membrane and denture hygiene habits. The guidelines for care and maintenance of dentures for COPD patients are presented in this paper. The majority of patients required improvement of their prosthetic and oral hygiene. Standard oral hygiene procedures in relation to dentures, conducted for prophylaxis of stomatitis complicated by mucosal infection among immunocompromised patients, are essential to maintain healthy oral tissues. The elimination of traumatic denture action in dental office, compliance with oral and denture hygiene, proper use and storage of prosthetic appliances in a dry environment outside the oral cavity can reduce susceptibility to infection. Proper attention to hygiene, including brushing and rinsing the mouth, may also help prevent denture stomatitis in these patients. PMID:25820669

  3. Acute effects of riociguat in borderline or manifest pulmonary hypertension associated with chronic obstructive pulmonary disease

    Ghofrani, Hossein A.; Staehler, Gerd; Grünig, Ekkehard; Halank, Michael; Mitrovic, Veselin; Unger, Sigrun; Mueck, Wolfgang; Frey, Reiner; Grimminger, Friedrich; Ralph T. Schermuly; Behr, Juergen

    2015-01-01

    Riociguat is the first oral soluble guanylate cyclase stimulator shown to improve pulmonary hemodynamics in patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension (PH). This pilot study assessed the impact of a single dose of riociguat on hemodynamics, gas exchange, and lung function in patients with PH associated with chronic obstructive pulmonary disease (COPD). Adults with COPD-associated borderline or manifest PH (pulmonary vascular resistance > 27...

  4. Systemic biomarkers of inflammation and haemostasis in patients with chronic necrotizing pulmonary aspergillosis

    Rødland Ernst

    2012-06-01

    Full Text Available Abstract Background The purpose of this study was to investigate mediators of inflammation and haemostasis in patients with chronic necrotizing pulmonary aspergillosis (CNPA, a locally, destructive process of the lung due to invasion by Aspergillus species. Methods Measurements of selected biomarkers in 10 patients with CNPA and 19 healthy, matched controls were performed with enzyme-linked immunosorbent assay (ELISA and multiplex methodology. The gene expressions of relevant biomarkers were analyzed with real-time quantitative RT-PCR. Results Increased concentrations of circulating mediators of inflammation interleukin (IL-6, IL-8, RANTES, TNF-α, ICAM-1 and mediators involved in endothelial activation and thrombosis (vWF, TF and PAI-1 were observed in patients with CNPA. The concentration of the anti-inflammatory cytokine IL-10 was increased both in plasma and in PBMC in the patient population. The gene expression of CD40L was decreased in PBMC from the patient group, accompanied by decreased concentrations of soluble (s CD40L in the circulation. Conclusions The proinflammatory response against Aspergillus may be counteracted by reduced CD40L and sCD40L, as well as increased IL-10, which may compromise the immune response against Aspergillus in patients with CNPA.

  5. Acute lung injury: How macrophages orchestrate resolution of inflammation and tissue repair

    Susanne eHerold

    2011-11-01

    Full Text Available Lung macrophages are long living cells with broad differentiation potential, which reside in the lung interstitium and alveoli or are organ-recruited upon inflammatory stimuli. A role of resident and recruited macrophages in initiating and maintaining pulmonary inflammation in lung infection or injury has been convincingly demonstrated. More recent reports suggest that lung macrophages are main orchestrators of termination and resolution of inflammation and initiators of parenchymal repair processes that are essential for return to homeostasis with normal gas exchange. In this review we will discuss cellular cross-talk mechanisms and molecular pathways of macrophage plasticity which define their role in inflammation resolution and in initiation of lung barrier repair following lung injury.

  6. Acute pulmonary injury: high-resolution CT and histopathological spectrum

    Obadina, E T; Torrealba, J M; Kanne, J P

    2013-01-01

    Acute lung injury usually causes hypoxaemic respiratory failure and acute respiratory distress syndrome (ARDS). Although diffuse alveolar damage is the hallmark of ARDS, other histopathological patterns of injury, such as acute and fibrinoid organising pneumonia, can be associated with acute respiratory failure. Acute eosinophilic pneumonia can also cause acute hypoxaemic respiratory failure and mimic ARDS. This pictorial essay reviews the high-resolution CT findings of acute lung injury and ...

  7. Longitudinal study of a mouse model of chronic pulmonary inflammation using breath hold gated micro-CT

    To evaluate the feasibility of using automatic quantitative analysis of breath hold gated micro-CT images to detect and monitor disease in a mouse model of chronic pulmonary inflammation, and to compare image-based measurements with pulmonary function tests and histomorphometry. Forty-nine A/J mice were used, divided into control and inflammation groups. Chronic inflammation was induced by silica aspiration. Fourteen animals were imaged at baseline, and 4, 14, and 34 weeks after silica aspiration, using micro-CT synchronized with ventilator-induced breath holds. Lung input impedance was measured as well using forced oscillation techniques. Five additional animals from each group were killed after micro-CT for comparison with histomorphometry. At all time points, micro-CT measurements show statistically significant differences between the two groups, while first differences in functional test parameters appear at 14 weeks. Micro-CT measurements correlate well with histomorphometry and discriminate diseased and healthy groups better than functional tests. Longitudinal studies using breath hold gated micro-CT are feasible on the silica-induced model of chronic pulmonary inflammation, and automatic measurements from micro-CT images correlate well with histomorphometry, being more sensitive than functional tests to detect lung damage in this model. (orig.)

  8. Noninvasive ventilation in patients with acute cardiogenic pulmonary edema

    Andrea Bellone

    2013-07-01

    Full Text Available The term noninvasive ventilation (NIV encompasses two different modes of delivering positive airway pressure, namely continuous positive airway pressure (CPAP and bilevel positive airway pressure (bilevel-PAP. The two modes are different since CPAP does not actively assist inspiration whereas bilevel-PAP does. Bilevel-PAP is a type of noninvasive ventilation that helps keep the upper airways of the lungs open by providing a flow of air delivered through a face mask. The air is pressurized by a machine, which delivers it to the face mask through long, plastic hosing. With bilevel-PAP, the doctor prescribes specific alternating pressures: a higher pressure is used to breathe in (inspiratory positive airway pressure and a lower pressure is used to breath out (expiratory positive airway pressure. Noninvasive ventilation has been shown to reduce the rate of tracheal intubation. The main indications are exacerbation of chronic obstructive pulmonary disease and acute cardiogenic pulmonary edema (ACPE. This last is a common cause of respiratory failure with high incidence and high mortality rate. Clinical findings of ACPE are related to the increased extra-vascular water in the lungs and the resulting reduced lung compliance, increased airway resistance and elevated inspiratory muscle load which generates a depression in pleural pressure. These large pleural pressure swings are responsible for hemodynamic changes by increasing left ventricular afterload, myocardial transmural pressure, and venous return. These alterations can be detrimental to patients with left ventricular systolic dysfunction. Under these circumstances, NIV, either by CPAP or bilevel-PAP, improves vital signs, gas exchange, respiratory mechanics and hemodynamics by reducing left ventricular afterload and preload. In the first randomized study which compared the effectiveness of CPAP plus medical treatment vs medical treatment alone, the CPAP group showed a significant decrease in its

  9. Outcomes of Noninvasive Ventilation for Acute Exacerbations of Chronic Obstructive Pulmonary Disease in the United States, 1998–2008

    Chandra, Divay; Stamm, Jason A.; Taylor, Brian; Ramos, Rose Mary; Satterwhite, Lewis; Krishnan, Jerry A.; Mannino, David; Sciurba, Frank C.; Holguín, Fernando

    2012-01-01

    Rationale: The patterns and outcomes of noninvasive, positive-pressure ventilation (NIPPV) use in patients hospitalized for acute exacerbations of chronic obstructive pulmonary disease (COPD) nationwide are unknown.

  10. Risk-Adapted Management of Acute Pulmonary Embolism: Recent Evidence, New Guidelines

    Anja Käberich; Simone Wärntges; Stavros Konstantinides

    2014-01-01

    Venous thromboembolism (VTE), the third most frequent acute cardiovascular syndrome, may cause life-threatening complications and imposes a substantial socio-economic burden. During the past years, several landmark trials paved the way towards novel strategies in acute and long-term management of patients with acute pulmonary embolism (PE). Risk stratification is increasingly recognized as a cornerstone for an adequate diagnostic and therapeutic management of the highly heterogeneous populati...

  11. Serum microRNA-1233 is a specific biomarker for diagnosing acute pulmonary embolism

    Kessler, Thorsten; Erdmann, Jeanette; Vilne, Baiba; Bruse, Petra; Kurowski, Volkhard; Diemert, Patrick; Schunkert, Heribert; Sager, Hendrik B

    2016-01-01

    Background Circulating microRNAs (miRNAs) emerge as novel biomarkers in cardiovascular diseases. Diagnosing acute pulmonary embolism (PE) remains challenging due to a diverse clinical presentation and the lack of specific biomarkers. Here we evaluate serum miRNAs as potential biomarkers in acute PE. Methods We enrolled 30 patients with acute, CT (computed tomography)-angiographically confirmed central PE and collected serum samples on the day of emergency room admission (1st day) and from 22 ...

  12. Acute lung inflammation induced in the rabbit by local instillation of 1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine or of native platelet-activating factor.

    Camussi, G.; Pawlowski, I.; Tetta, C; Roffinello, C.; Alberton, M.; Brentjens, J.; Andres, G.

    1983-01-01

    The intratracheal instillation into rabbits of 1-0-octadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (AGEPC) or native platelet-activating factor (PAF) was shown to induce a dose-dependent acute pulmonary inflammation characterized by accumulation of macrophages in the alveolar space, degenerative and necrotic changes of alveolar epithelium, and accumulation of polymorphonuclear leukocytes (PMNs) and platelets in the alveolar capillary lumens with degenerative changes of endothelial cells. I...

  13. Acute effect of tetrandrine pulmonary targeting microspheres on hypoxic pulmonary hypertension in rats

    程德云; 陈文彬; 莫晓能

    2002-01-01

    Objective To assess the effect of tetrandrine (Tet) pulmonary targeting microspheres on hypoxic pulmonary hypertension and evaluate its selective action on pulmonary circulation. Methods Twenty rats were exposed to hypoxic conditions for 3 weeks. Ten rats were used as normoxic controls. We administered Tet pulmonary targeting microspheres to 10 hypoxic rats and Tet aqueous solution to 10 hypoxic rats and the 10 control rats. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization, and mean systemic blood pressure (mSBP) was measured by left femoral catheterization. Results Rats exposed to hypoxia developed pulmonary hypertension. The decrease in mPAP in rats treated with Tet pulmonary targeting microspheres was significantly greater than that in rats receiving Tet aqueous solution (P<0.05), and the effects were longer with Tet pulmonary targeting microspheres. Moreover, Tet pulmonary targeting microspheres, unlike Tet aqueous solution, did not decrease mSBP. Conclusion Tet pulmonary targeting microspheres were more effective than Tet aqueous solution in treating hypoxic pulmonary hypertension and acted selectively on the pulmonary circulation.

  14. Widening of coronary sinus in CT pulmonary angiography indicates right ventricular dysfunction in patients with acute pulmonary embolism

    Right ventricular dysfunction (RVD) may occur in the course of acute pulmonary embolism (PE). Patients with RVD need more intensive treatment, and the prognosis is more severe. The aim of this study was to evaluate the usefulness of the measurement of the coronary sinus in the assessment of RVD in patients with acute PE and to compare it with other indicators of RVD. Retrospective assessment of 55 CT pulmonary angiography examinations with signs of acute PE was performed. Pulmonary artery systolic pressure (PASP) was echocardiographically assessed in all patients, and RVD was defined as PASP values greater than 30 mmHg. CT measurements included the size of the heart ventricles, mediastinal vessels and the width of the coronary sinus. Median width of the coronary sinus was 16 mm (range 12-24 mm) in patients with increased PASP and 10 mm (range 7-22 mm) in patients with normal PASP (p = 0.001). Best cut-off value was assessed to be 12.5 mm, with sensitivity 94% and specificity 75%. It was characterised by the largest area under ROC curve (0.82) among analysed parameters. Width of the coronary sinus seems to be a promising parameter for identification of RVD in patients with acute PE. A prospective study should be undertaken to further assess its clinical and prognostic applicability. (orig.)

  15. Interleukin 6 and lipopolysaccharide binding protein - markers of inflammation in acute appendicitis.

    Brănescu, C; Serban, D; Dascălu, A M; Oprescu, S M; Savlovschi, C

    2013-01-01

    The rate of incidence of acute appendicitis is 12% in the case of male patients and 25% in case of women, which represents about 7% of the world population. The appendectomy rate has remained constant (i.e. 10 out of 10,000 patients per year). Appendicitis most often occurs in patients aged between 11-40 years, on the threshold between the third and fourth decades, the average age being 31.3 years. Since the first appendectomy performed by Claudius Amyand (1681/6 -1740), on December, 6th, 1735 to our days, i.e., 270 years later, time has confirmed the efficiency of both the therapy method and the surgical solution. The surgical cure in case of acute appendicitis has proved to be acceptable within the most widely practised techniques in general surgery. The variety of clinical forms has reached all age ranges, which in its turn has resulted in a large number of semiotic signs. In the case of acute appendicitis, interdisciplinarity has allowed the transfer of concept and methodology transfer among many areas of expertise, aimed at a better, minute understanding of the inflammatory event itself. Acute appendicitis illustrates inflammation development at digestive level and provides for a diagnostic and paraclinical exploration which continually upgrades. The recent inclusion in the studies of the Lipopolysaccharide binding protein (LBP)- type inflammation markers has laid the foundation of the latter's documented presence in the case of acute appendicitis-related inflammation. Proof of the correlation between the histopathological, clinical and evolutive forms can be found by identifying and quantifying these inflammation markers. The importance of studying inflammation markers allows us to conduct studies going beyond the prognosis of the various stages in which these markers were identified. The present article shows the results of a 1-year monitoring of the inflammation markers' values for Interleukin-6 and Lipopolysaccharide binding protein (LBP)-types, both pre

  16. Lung transcriptional profiling: insights into the mechanisms of ozone-induced pulmonary injury in Wistar Kyoto rats

    Acute ozone-induced pulmonary injury and inflammation are well characterized in rats; however, mechanistic understanding of the pathways involved is limited. We hypothesized that acute exposure of healthy rats to ozone will cause transcriptional alterations, and comprehensive ana...

  17. Metabolic reprogramming and inflammation act in concert to control vascular remodeling in hypoxic pulmonary hypertension.

    Stenmark, Kurt R; Tuder, Rubin M; El Kasmi, Karim C

    2015-11-15

    Pulmonary hypertension (PH) is a complex, multifactorial syndrome that remains poorly understood despite decades of research. PH is characterized by profound pulmonary artery (PA) remodeling that includes significant fibro-proliferative and inflammatory changes of the PA adventitia. In line with the emerging concept that PH shares key features with cancer, recent work centers on the idea that PH results from a multistep process driven by reprogramming of gene-expression patterns that govern changes in cell metabolism, inflammation, and proliferation. Data demonstrate that in addition to PA endothelial cells and smooth muscle cells, adventitial fibroblasts from animals with experimental hypoxic PH and from humans with PH (hereafter, termed PH-Fibs) exhibit proinflammatory activation, increased proliferation, and apoptosis resistance, all in the context of metabolic reprogramming to aerobic glycolysis. PH-Fibs can also recruit, retain, and activate naïve macrophages (Mϕ) toward a proinflammatory/proremodeling phenotype through secretion of chemokines, cytokines, and glycolytic metabolites, among which IL-6 and lactate play key roles. Furthermore, these fibroblast-activated Mϕ (hereafter, termed FAMϕ) exhibit aerobic glycolysis together with high expression of arginase 1, Vegfa, and I1lb, all of which require hypoxia-inducible factor 1α and STAT3 signaling. Strikingly, in situ, the adventitial Mϕ phenotype in the remodeled PA closely resembles the Mϕ phenotype induced by fibroblasts in vitro (FAMϕ), suggesting that FAMϕ crosstalk involving metabolic and inflammatory signals is a critical, pathogenetic component of vascular remodeling. This review discusses metabolic and inflammatory changes in fibroblasts and Mϕ in PH with the goal of raising ideas about new interventions to abrogate remodeling in hypoxic forms of PH. PMID:25930027

  18. Pulmonary circulatory parameters as indices for the early detection of acute rejection after single lung transplantation.

    Yamamoto, H; Okada, M; Tobe, S; Tsuji, F; Ohbo, H; Nakamura, H; Yamashita, C

    1998-01-01

    We investigated the relationship between the changes in the pulmonary blood flow and histology during acute rejection following single lung transplantation. In single lung transplantation using adult mongrel dogs, immunosuppression with cyclosporine and azathioprine was discontinued after postoperative day 14 to induce rejection. Doppler flow probes were placed adjacent to the ascending aorta and the left pulmonary artery to measure the blood flow on a daily basis. In addition, chest roentgenograms were also examined daily. The pulmonary pressure was measured using a Swan-Ganz catheter prior to and following the induction of rejection. Open lung biopsies were performed when the left pulmonary artery flow decreased to half of the prerejection value. The pulmonary artery flow decreased to 14.3% of the aortic flow 5 days after the discontinuation of immunosuppression. The graft pulmonary vascular resistance increased significantly compared to the prerejection values (P < 0.001). This was not accompanied by any abnormalities on chest roentgenography. The histology was consistent, with marked perivascular lymphocytic infiltration with little alveolar or interstitial changes. During rejection, the increased pulmonary vascular resistance in the graft was probably the result of perivascular inflammatory cell infiltration, which was seen prior to changes on chest roentgenography. Changes in the left pulmonary artery flow and histology thus appear to be closely correlated in the early stages of acute rejection. PMID:9744398

  19. Effect of trimetazidine on acute and sub-acute models of inflammation in male wistar rats

    Naveena R

    2016-06-01

    Conclusions: Results of the study indicate that trimetazidine can reduce the complications of atherosclerosis which involves inflammation as the major steps in its pathogenesis. [Int J Basic Clin Pharmacol 2016; 5(3.000: 782-787

  20. SCREENING OF THE ANTIINFLAMMATORY ACTIVITY OF “TRIANTHEMA PORTULACASTRUM” IN ACUTE MODELS OF INFLAMMATION

    Suresh S

    2015-04-01

    Full Text Available BACKGROUND : There are many anti - inflammatory drugs available but all of them do have a significant adverse effect profile. Trianthema portulacastrum is known in Ayurveda since centuries for its medicinal values. So the current study was underta ken to evaluate the anti - inflammatory effects of this plant in acute inflammation. MATERIALS AND METHOD S : Albino rats were treated with whole plant ethonolic extract of Trianthema portulacastrum 100mg \\ kg, indomethacin 20 mg \\ kg, orally with 2% gum acacia as suspending agent and the effects were observed in acute models of inflammation viz, carrrageenin induced paw edema and formalin induced peritonitis. RESULTS : our study demonstrated that Trianthema portulacastrum exhibited significant anti - inflammatory activity in both the models. CONCLUSION : Trianthema potrulacastum has got significant anti - inflammatory activity so further studies are needed in this direction.

  1. Acute hyperammonemia and systemic inflammation is associated with increased extracellular brain adenosine in rats

    Bjerring, Peter Nissen; Dale, Nicholas; Larsen, Fin Stolze

    2015-01-01

    Acute liver failure (ALF) can lead to brain edema, cerebral hyperperfusion and intracranial hypertension. These complications are thought to be mediated by hyperammonemia and inflammation leading to altered brain metabolism. As increased levels of adenosine degradation products have been found in...... cerebral blood flow (CBF). We measured the adenosine concentration with biosensors in rat brain slices exposed to ammonia and in a rat model with hyperammonemia and systemic inflammation. Exposure to ammonia in concentrations from 0.15-10 mM led to increases in the cortical adenosine concentration up to 18...... µM in brain slices. In vivo recordings showed a tendency towards increased adenosine levels in rats with hyperammonemia and systemic inflammation compared to a control group (3.7 ± 0.7 vs. 0.8 ± 0.2 µM, P = 0.06). This was associated with a significant increase in ICP and CBF. Intervention with the...

  2. TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins

    Meseguer, Victor; Alpizar, Yeranddy A.; Luis, Enoch; Tajada, Sendoa; Denlinger, Bristol; Fajardo, Otto; Manenschijn, Jan-Albert; Fernández-Peña, Carlos; Talavera, Arturo; Kichko, Tatiana; Navia, Belén; Sánchez, Alicia; Señarís, Rosa; Reeh, Peter; Pérez-García, María Teresa; López-López, José Ramón; Voets, Thomas; Belmonte, Carlos; Talavera, Karel; Viana, Félix

    2014-01-01

    Gram-negative bacterial infections are accompanied by inflammation and somatic or visceral pain. These symptoms are generally attributed to sensitization of nociceptors by inflammatory mediators released by immune cells. Nociceptor sensitization during inflammation occurs through activation of the Toll-like receptor 4 (TLR4) signalling pathway by lipopolysaccharide (LPS), a toxic by-product of bacterial lysis. Here we show that LPS exerts fast, membrane delimited, excitatory actions via TRPA1, a transient receptor potential cation channel that is critical for transducing environmental irritant stimuli into nociceptor activity. Moreover, we find that pain and acute vascular reactions, including neurogenic inflammation (CGRP release) caused by LPS are primarily dependent on TRPA1 channel activation in nociceptive sensory neurons, and develop independently of TLR4 activation. The identification of TRPA1 as a molecular determinant of direct LPS effects on nociceptors offers new insights into the pathogenesis of pain and neurovascular responses during bacterial infections and opens novel avenues for their treatment.

  3. The acute impact of a hematopoietic allograft on lung function and inflammation: a prospective observational study

    Enocson Alexandra

    2013-01-01

    Full Text Available Abstract Background No studies have investigated the immediate impact of receiving an allogeneic hematopoietic stem cell transplant (HSCT on pulmonary inflammation or lung function. Methods Using a prospective study design, we quantified the changes in these outcome measures in eligible adult individuals in the first six months after receiving an allogeneic hematopoietic stem cell transplant. Results Between January 2007 and December 2008, 72 patients were eligible to participate in the cohort, and of these 68 (94% were included in the study. Compared to baseline, pulmonary inflammation as measured by exhaled nitric oxide increased after receiving a HSCT with the largest increment seen at three months (+6.0ppb, 95%CI: +0.4 to +11.5, and this was sustained at six months. Percent predicted forced expiratory volume in one second decreased over the same period, with the largest decrease observed at six weeks (−5.9%, 95% CI: -8.9 to −2.9, and this was also sustained over a six month period. Similar associations were observed for FVC. A larger increase in exhaled nitric oxide from baseline at six weeks and three months may be associated with decreased mortality (p=0.06, p=0.04 respectively. Conclusion Our data demonstrate that recipients of an allogeneic HSCT experience an increase in biomarkers of pulmonary inflammation and a decrease in lung function in the first six months after the procedure. If independently validated in other study populations, these observations could have potential as a prognostic biomarker for this patient group.

  4. Intratendinous Injection of Hyaluronate Induces Acute Inflammation: A Possible Detrimental Effect

    Wu, Po-Ting; Jou, I-Ming; Kuo, Li-Chieh; Su, Fong-Chin

    2016-01-01

    Hyaluronate (HA) is therapeutic for tendinopathy, but an intratendinous HA injection is usually painful; thus, it is not suggested for clinical practice. However, there are no studies on the histopathological changes after an intratendinous HA injection. We hypothesized that an HA injection would induce more-acute inflammation than that induced by an injection of phosphate buffered saline (PBS). Thirty-two rats were randomly divided into 4 post-injection groups (n = 8): day 3, day 7, day 28, ...

  5. Myeloid tissue factor does not modulate lung inflammation or permeability during experimental acute lung injury

    Shaver, Ciara M.; Grove, Brandon S.; Clune, Jennifer K.; Nigel Mackman; Lorraine B. Ware; Bastarache, Julie A

    2016-01-01

    Tissue factor (TF) is a critical mediator of direct acute lung injury (ALI) with global TF deficiency resulting in increased airspace inflammation, alveolar-capillary permeability, and alveolar hemorrhage after intra-tracheal lipopolysaccharide (LPS). In the lung, TF is expressed diffusely on the lung epithelium and intensely on cells of the myeloid lineage. We recently reported that TF on the lung epithelium, but not on myeloid cells, was the major source of TF during intra-tracheal LPS-indu...

  6. The Resolution Code of Acute Inflammation: Novel Pro-Resolving Lipid Mediators in Resolution

    Serhan, Charles N.; Chiang, Nan; Dalli, Jesmond

    2015-01-01

    Studies into the mechanisms in resolution of self-limited inflammation and acute reperfusion injury have uncovered a new genus of pro-resolving lipid mediators coined specialized pro-resolving mediators (SPM) including lipoxins, resolvins, protectins and maresins that are each temporally produced by resolving-exudates with distinct actions for return to homeostasis. SPM evoke potent anti-inflammatory and novel pro-resolving mechanisms as well as enhance microbial clearance. While born in infl...

  7. Novel lipid mediators promote resolution of acute inflammation: impact of aspirin and statins

    Spite, Matthew; Serhan, Charles N.

    2010-01-01

    The resolution of acute inflammation is a process that allows for inflamed tissues to return to homeostasis. Resolution was held to be a passive process, a concept now overturned with new evidence demonstrating that resolution is actively orchestrated by distinct cellular events and endogenous chemical mediators. Among these, lipid mediators, such as the lipoxins, resolvins, protectins and newly identified maresins, have emerged as a novel genus of potent and stereoselective players that coun...

  8. Peroxisome proliferator-activated receptor gamma as modulator of inflammation in pulmonary sarcoidosis

    Pejčić Tatjana

    2013-01-01

    Full Text Available Peroxisome proliferator-activated receptor (PPAR includes the family of ligand-activated transcription factors which belong to the group of nuclear hormone receptors and are connected to retinoid, glucocorticoid and thyroid hormone receptors. There are three subtypes of PPARs: PPARα (also known as NR1C3, PPARγ (known as NR1C1 and PPARδ (known as PPARβ or NR1C2. All of them take part in the metabolism, cell proliferation and immune response. PPARγ and PPARα are identified as important immunomodulators and potentially represent an anti-inflammatory target for respiratory diseases. PPARγ deficiency in the lungs has been observed in the inflammatory diseases such as asthma, pulmonary alveolar proteinosis, fibrosis and sarcoidosis, as well as in the animal models of the lung inflammation. A small number of papers concerned with PPARγ in sarcoidosis point to the lowered activity of this factor in the alveolar macrophages and a lowered gene expression for the PPARγ, while the activity is preserved in healthy individuals. At the same time, an increased activity of the nuclear factor kappa B (NF-kB in the bronchoalveolar lavage has been recorded in patients with sarcoidosis. The reason for the decrease in the production of PPARγ in sarcoidosis remains unknown. Several possible mechanisms are mentioned: genetic defect with lowered production, down-regulation due to the increased values of IFN-γ or an increased decomposition of PPARγ. Further investigation will explain the mechanisms regarding the decreased production of PPARγ in sarcoidosis.

  9. Hirsutella sinensis mycelium attenuates bleomycin-induced pulmonary inflammation and fibrosis in vivo.

    Huang, Tsung-Teng; Lai, Hsin-Chih; Ko, Yun-Fei; Ojcius, David M; Lan, Ying-Wei; Martel, Jan; Young, John D; Chong, Kowit-Yu

    2015-01-01

    Hirsutella sinensis mycelium (HSM), the anamorph of Cordyceps sinensis, is a traditional Chinese medicine that has been shown to possess various pharmacological properties. We previously reported that this fungus suppresses interleukin-1β and IL-18 secretion by inhibiting both canonical and non-canonical inflammasomes in human macrophages. However, whether HSM may be used to prevent lung fibrosis and the mechanism underlying this activity remain unclear. Our results show that pretreatment with HSM inhibits TGF-β1-induced expression of fibronectin and α-SMA in lung fibroblasts. HSM also restores superoxide dismutase expression in TGF-β1-treated lung fibroblasts and inhibits reactive oxygen species production in lung epithelial cells. Furthermore, HSM pretreatment markedly reduces bleomycin-induced lung injury and fibrosis in mice. Accordingly, HSM reduces inflammatory cell accumulation in bronchoalveolar lavage fluid and proinflammatory cytokines levels in lung tissues. The HSM extract also significantly reduces TGF-β1 in lung tissues, and this effect is accompanied by decreased collagen 3α1 and α-SMA levels. Moreover, HSM reduces expression of the NLRP3 inflammasome and P2X7R in lung tissues, whereas it enhances expression of superoxide dismutase. These findings suggest that HSM may be used for the treatment of pulmonary inflammation and fibrosis. PMID:26497260

  10. Observations on the mechanism of hypoxaemia in acute minor pulmonary embolism.

    Burton, G H; Seed, W A; Vernon, P.

    1984-01-01

    An automated computer analysis of ventilation-perfusion lung scans was used to derive graphical data from lung scans of 11 patients with acute minor pulmonary embolism, free of pre-existing cardiorespiratory disease, and with no evidence of intrapulmonary complication or pleural effusion. In each case the analysis showed the presence of areas of lung, remote from those affected by the pulmonary embolism, that had a pathological disturbance of ventilation-perfusion matching with relative overp...

  11. Diffuse Pulmonary Hemorrhage After Fibrinolytic Therapy for Acute Myocardial Infarction in a Cocaine Abuser Patient

    Mohammad Parsa Mahjoob; Isa Khaheshi; Koosha Paydary

    2014-01-01

    We report a 45-year-old man with antroseptal myocardial infarction who developed bilateral basal alveolar infiltrates after initiating the fibrinolytic therapy. Although thrombolytic therapy with streptokinase is generally used in the course of acute myocardial infarction and has diminished morbidity and mortality, pulmonary hemorrhage is an uncommon, but a potentially life-threatening complication that should be regarded as one of the differential diagnoses of pulmonary infiltrates or droppi...

  12. Acute pulmonary embolism caused by enlarged uterine leiomyoma: A rare presentation

    Khademvatani, Kamal; Rezaei, Yousef; Kerachian, Abdollah; Seyyed-Mohammadzad, Mir Hossein; Eskandari, Ramin; Rostamzadeh, Alireza

    2014-01-01

    Patient: Female, 42 Final Diagnosis: Acute pulmonary embolism Symptoms: Chest pain • dyspnea Medication: Streptokinase • Warfarin Clinical Procedure: — Specialty: Cardiology and Neoplasm Objective: Management of emergency care Background: Deep venous thrombosis (DVT) and subsequent pulmonary embolism (PE) caused by pelvic vein compression are rare and life-threatening complications of leiomyoma of the uterus. Case Report: We report a 42-year-old virgin woman with a history of leiomyoma who pr...

  13. Markers of acute-phase response in the treatment of pulmonary tuberculosis

    Cristiane Martins; Antônio Carlos de Castro Gama; Daniela Valcarenghi; Anna Paula de Borba Batschauer

    2014-01-01

    Introduction:Tuberculosis promotes an acute phase response with an increase of blood reactants, such as C-reactive protein (CRP), among others, which are associated with increased erythrocyte sedimentation rate (ESR).Objective:Evaluate the ESR and the CRP as markers for diagnosis and monitoring cases of pulmonary tuberculosis.Method:Research on patients with clinical, laboratory, and imaging diagnosis of pulmonary tuberculosis, from Itajaí-SC; in which CRP and ESR were analyzed in three diffe...

  14. Pulse pressure variation and volume responsiveness during acutely increased pulmonary artery pressure: an experimental study

    Daudel, Fritz; Tüller, David; Krähenbühl, Stefanie; Jakob, Stephan M; Takala, Jukka

    2010-01-01

    Introduction We found that pulse pressure variation (PPV) did not predict volume responsiveness in patients with increased pulmonary artery pressure. This study tests the hypothesis that PPV does not predict fluid responsiveness during an endotoxin-induced acute increase in pulmonary artery pressure and right ventricular loading. Methods Pigs were subjected to endotoxemia (0.4 μg/kg/hour lipopolysaccharide), followed by volume expansion, subsequent hemorrhage (20% of estimated blood volume), ...

  15. IL-17A is essential to the development of elastase-induced pulmonary inflammation and emphysema in mice

    Kurimoto Etsuko

    2013-01-01

    Full Text Available Abstract Background Pulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. Although IL-17A contributes to many chronic inflammatory diseases, it’s role in the inflammatory response of elastase-induced emphysema remains unclear. Methods In a model of elastase-induced pulmonary emphysema we examined the response of IL-17A-deficient mice, monitoring airway inflammation, static compliance, lung histology and levels of neutrophil-related chemokine and pro-inflammatory cytokines in bronchoalveolar lavage (BAL fluid. Results Wild-type mice developed emphysematous changes in the lung tissue on day 21 after elastase treatment, whereas emphysematous changes were decreased in IL-17A-deficient mice compared to wild-type mice. Neutrophilia in BAL fluid, seen in elastase-treated wild-type mice, was reduced in elastase-treated IL-17A-deficient mice on day 4, associated with decreased levels of KC, MIP-2 and IL-1 beta. Elastase-treated wild-type mice showed increased IL-17A levels as well as increased numbers of IL-17A+ CD4 T cells in the lung in the initial period following elastase treatment. Conclusions These data identify the important contribution of IL-17A in the development of elastase-induced pulmonary inflammation and emphysema. Targeting IL-17A in emphysema may be a potential therapeutic strategy for delaying disease progression.

  16. Therapeutic expansion of CD4+FoxP3+ regulatory T cells limits allergic airway inflammation during pulmonary fungal infection.

    Schulze, Bianca; Piehler, Daniel; Eschke, Maria; Heyen, Laura; Protschka, Martina; Köhler, Gabriele; Alber, Gottfried

    2016-06-01

    Allergic asthma can be frequently caused and exacerbated by sensitization to ubiquitous fungal allergens associated with pulmonary mucus production, airway hyperresponsiveness and bronchial constriction, resulting in a complex disease that is often difficult to treat. Fungal infections are frequently complicated by the development of a type 2 immune response that prevents successful elimination of the fungal pathogen. Furthermore, production of type 2 cytokines triggers allergic airway inflammation. Following intranasal infection of BALB/c mice with the fungusCryptococcus neoformans, we recently described a more pronounced type 2 immune response in the absence of regulatory T (Treg) cells. To determine whether Treg cell expansion is able to suppress type 2-related fungal allergic inflammation, we increased Treg cell numbers during pulmonaryC. neoformansinfection by administration of an interleukin (IL)-2/anti-IL-2 complex. Expansion of Treg cells resulted in reduced immunoglobulin E production and decreased allergic airway inflammation including reduced production of pulmonary mucus and type 2 cytokines as well as production of immunosuppressive cytokines such as IL-10 and transforming growth factor-β1. From our data we conclude that Treg cells and/or their suppressive mediators represent potential targets for therapeutic intervention during allergic fungal airway disease. PMID:27001975

  17. Attenuation of Acute Lung Inflammation and Injury by Whole Body Cooling in a Rat Heatstroke Model

    Hsi-Hsing Yang

    2009-01-01

    Full Text Available Whole body cooling is the current therapy of choice for heatstroke because the therapeutic agents are not available. In this study, we assessed the effects of whole body cooling on several indices of acute lung inflammation and injury which might occur during heatstroke. Anesthetized rats were randomized into the following groups and given (a no treatment or (b whole body cooling immediately after onset of heatstroke. As compared with the normothermic controls, the untreated heatstroke rats had higher levels of pleural exudates volume and polymorphonuclear cell numbers, lung myloperoxidase activity and inducible nitric oxide synthase expression, histologic lung injury score, and bronchoalveolar proinflammatory cytokines and glutamate, and PaCO2. In contrast, the values of mean arterial pressure, heart rate, PaO2, pH, and blood HCO3− were all significantly lower during heatstroke. The acute lung inflammation and injury and electrolyte imbalance that occurred during heatstroke were significantly reduced by whole body cooling. In conclusion, we identified heat-induced acute lung inflammation and injury and electrolyte imbalance could be ameliorated by whole body cooling.

  18. The central role of hypothalamic inflammation in the acute illness response and cachexia.

    Burfeind, Kevin G; Michaelis, Katherine A; Marks, Daniel L

    2016-06-01

    When challenged with a variety of inflammatory threats, multiple systems across the body undergo physiological responses to promote defense and survival. The constellation of fever, anorexia, and fatigue is known as the acute illness response, and represents an adaptive behavioral and physiological reaction to stimuli such as infection. On the other end of the spectrum, cachexia is a deadly and clinically challenging syndrome involving anorexia, fatigue, and muscle wasting. Both of these processes are governed by inflammatory mediators including cytokines, chemokines, and immune cells. Though the effects of cachexia can be partially explained by direct effects of disease processes on wasting tissues, a growing body of evidence shows the central nervous system (CNS) also plays an essential mechanistic role in cachexia. In the context of inflammatory stress, the hypothalamus integrates signals from peripheral systems, which it translates into neuroendocrine perturbations, altered neuronal signaling, and global metabolic derangements. Therefore, we will discuss how hypothalamic inflammation is an essential driver of both the acute illness response and cachexia, and why this organ is uniquely equipped to generate and maintain chronic inflammation. First, we will focus on the role of the hypothalamus in acute responses to dietary and infectious stimuli. Next, we will discuss the role of cytokines in driving homeostatic disequilibrium, resulting in muscle wasting, anorexia, and weight loss. Finally, we will address mechanisms and mediators of chronic hypothalamic inflammation, including endothelial cells, chemokines, and peripheral leukocytes. PMID:26541482

  19. Quantification of right ventricular function in acute pulmonary embolism: relation to extent of pulmonary perfusion defects

    Kjaergaard, J.; Schaadt, B.K.; Lund, J.O.;

    2008-01-01

    Aims The relation of the extent of obstruction of the pulmonary vascutature in pulmonary embolism (PE) and impact on right ventricular (RV) hemodynamics is not well established. This study evaluated the relation of size of perfusion defects and changes in echocardiographic measures of global and...... regional RV dysfunction in 58 consecutive patients with non-massive PE. Methods and results Patients were compared with 58 age-matched controls that had normal ventilation/perfusion scintigraphies. A 2D, Doppler and Tissue Doppler echocardiography performed on the same day, quantified RV pressure and...... global and regional performance. Intermediate and large pulmonary emboli were associated with a significant impact on RV pressure and function. For small pulmonary emboli obstructing <25% of the pulmonary vascutature, the acceleration time of the pulmonary artery (PA) outflow was significantly shortened...

  20. Detection of experimentally produced acute pulmonary arterial occlusion by methyl iodide-131 inhalation imaging

    Methyl iodide-131 (CH3I-131) is described as an agent for detection of acute experimentally produced pulmonary arterial occlusion in dogs. When gaseous CH3I-131 is inhaled, radioactivity passes instantaneously from the alveoli to the lung capillary bed. Where pulmonary blood flow exists, activity is washed out into the systemic circulation, but in areas of blood stasis, a transient pulmonary hot spot remains. CH3I-131 is easily produced and inexpensive, but administration is awkward and strict radiation safety precautions are mandatory

  1. Acute respiratory distress syndrome caused by Mycoplasma pneumoniae without elevated pulmonary vascular permeability: a case report.

    Takahashi, Naoki; Shinohara, Tsutomu; Oi, Rie; Ota, Muneyuki; Toriumi, Shinichi; Ogushi, Fumitaka

    2016-05-01

    Sporadic patients with acute respiratory distress syndrome (ARDS) caused by Mycoplasma pneumoniae have been reported. However, knowledge about the pathophysiology and pharmacological treatment of this condition is insufficient. Moreover, the pulmonary vascular permeability in ARDS related to M. pneumoniae infection has not been reported. We report a case of ARDS caused by Mycoplasma pneumoniae without elevated pulmonary vascular permeability, which was successfully treated using low-dose short-term hydrocortisone, suggesting that pulmonary infiltration in ARDS caused by Mycoplasma pneumoniae does not match the criteria of permeability edema observed in typical ARDS. PMID:27162691

  2. Effect of early treatment with transcutaneous electrical diaphragmatic stimulation (TEDS on pulmonary inflammation induced by bleomycin

    Laisa A. Santos

    2013-12-01

    Full Text Available BACKGROUND : Bleomycin (B is an antineoplastic drug that has pulmonary fibrosis as a side effect. There are few experimental studies about the effects of physical therapy treatment in this case. OBJECTIVE: The objective was to study rat lungs treated with B and precocious intervention by transcutaneous electrical diaphragmatic stimulation (TEDS. METHOD : Wistar rats were divided into 4 groups (n=5: a control group (C; a stimulated group (TEDS; a group treated with a single dose of B (intratracheally, 2.5 mg/kg (B; and a group treated with B and electric stimulation (B + TEDS. After the B instillation, the electrical stimulation was applied for 7 days, for a duration of 20 minutes. Lung fragments were histologically processed with hematoxylin and eosin (HE and 8-isoprostane-PGF2α (8-iso-PGF2α. The density of the alveolar area was determined by planimetry, the inflammatory profile was defined by the number of cells, and the level of oxidative stress in the pulmonary tissue was evaluated by 8-iso-PGF2α. For statistical analysis of the data, the Shapiro-Wilk test was used, followed by a one-way ANOVA with the post-hoc Bonferroni test (p≤0.05. RESULTS : The B group exhibited a significant reduction in the area density, and the acute treatment with B + TEDS prevented this reduction. There were increased numbers of fibroblasts, leukocytes, and macrophages in the B group, as well as increased lipid peroxidation, which was observed only in this group. CONCLUSION : B promoted a reduction in the alveolar density area, thereby inducing the inflammatory process and increasing the production of free radicals. These effects were minimized by the application of TEDS at the initial treatment stage.

  3. Related research between right ventricular dysfunction and pulmonary embolism range of the patients with acute pulmonary thromboembolism

    Objective: The presence of right ventrieular dysfunction (RVD) increases morbidity and mortality of the patient with pulmonary thromboembolism (PTE). The aims of this study were to evaluate the relation between RVD on echocardiography and pulmonary embolism range on radionuclide palmonary ventilation-perfusion (V/Q) scan of the patients with acute PTE, and to discuss the diagnostic feasibility of RVD by pulmonary embolism range. Methods: All 348 patients with proven PTE were classified as two groups according to the echocardiography diagnosis. Two hundreds and twelve were with RVD and 136 were with normal right ventricular function (N-RVF). All underwent pulmonary V/Q imping.Statistical analysis was performed with SPSS 11.5, and the relation between RVD and pulmonary embolism range was performed with χ2 analysis, correlation analysis, receiver operating characteristic (ROC) curve analysis. Results: Signiticant relations between RVD (right/left ventricular end-diastolic diameter ratio (RVD/LVD)=0.52 ± 0.22. right/left ventricular transverse diameter ratio (RVTD/LVTD) =0.88 ± 0.26, tricuspid regurgitant pressure gradient (TRPG) = (31.93 ± 21.79) nun Hg (1 mm Hg = 0.133 kPa) and right ventricular anterior wall moilon (RVAWM) = (5.77 ± 1.99) mm) and pulmonary embolism range (1 ∼ 36, 11.4 ± 7.1) RVF and RVD and larger embolism range in RVD than in N-RVF (χ2=445.93, P2.58, P<0.01. Conclusion: The pulmonary embolism area waft negatively correlated with the RVD and had potential of being one of the references for the impression of RVD in PTE patients. (authors)

  4. Pulmonary hydatid cyst in a pregnant patient causing acute respiratory failure

    Hijazi Mohammed

    2007-01-01

    Full Text Available A 21-year-old primigravida, at 32 weeks of gestation, presented with acute onset of respiratory failure and circulatory shock. Chest imaging showed findings suggestive of ruptured hydatid cyst, which was confirmed by histology post-thoracotomy. Tissue cultures from the removed cyst grew Mycobacterium tuberculosis also. She was successfully managed in the intensive care unit and was then discharged home on antituberculosis medications in addition to albendazole after prolonged hospitalization and a need for chest tube for bronchopleural fistula. Acute respiratory failure and anaphylactic shock secondary to ruptured pulmonary hydatid cyst and superimposed pulmonary tuberculosis in a pregnant lady should be considered in patients living in endemic areas.

  5. A Case of Fatal Acute Lung Injury after Balloon Valvuloplasty of Pulmonary Stenosis: Case Report and Review of Literature

    Ostovan Mohammad Ali; Kamali Maliheh; Zolghadrasli Abdolali

    2015-01-01

    A newly described immediate complication after percutaneous pulmonary valvuloplasty is acute lung injury. Here we report a case of fatal acute lung injury after pulmonary valvuloplasty.The patient was a 26-year-old woman, referred to a general hospital with the diagnosis of livercirrhosis. In her work-ups severe pulmonary stenosis was detected and so a decision was madeto relieve the valve stenosis. Despite the procedural success, the patient developed severe dyspneaand desaturation a few hou...

  6. The role of inflammation and interleukin-1 in acute cerebrovascular disease

    Galea J

    2013-08-01

    Full Text Available James Galea,1 David Brough21Manchester Academic Health Sciences Center, Brain Injury Research Group, Clinical Sciences Building, Salford Royal Foundation Trust, Salford, UK; 2Faculty of Life Sciences, University of Manchester, AV Hill Building, Manchester, UKAbstract: Acute cerebrovascular disease can affect people at all stages of life, from neonates to the elderly, with devastating consequences. It is responsible for up to 10% of deaths worldwide, is a major cause of disability, and represents an area of real unmet clinical need. Acute cerebrovascular disease is multifactorial with many mechanisms contributing to a complex pathophysiology. One of the major processes worsening disease severity and outcome is inflammation. Pro-inflammatory cytokines of the interleukin (IL-1 family are now known to drive damaging inflammatory processes in the brain. The aim of this review is to discuss the recent literature describing the role of IL-1 in acute cerebrovascular disease and to provide an update on our current understanding of the mechanisms of IL-1 production. We also discuss the recent literature where the effects of IL-1 have been targeted in animal models, thus reviewing potential future strategies that may limit the devastating effects of acute cerebrovascular disease.Keywords: cerebral ischemia, stroke, inflammation, microglia, interleukin-1, caspase-1

  7. Is there a place for inhaled nitric oxide in the therapy of acute pulmonary embolism?

    Tanus-Santos, Jose E; Theodorakis, Michael J

    2002-01-01

    Acute pulmonary embolism (PE) is a serious complication resulting from the migration of emboli to the lungs. Although deep venous thrombi are the most common source of emboli to the lungs, other important sources include air, amniotic fluid, fat and bone marrow. Regardless of the specific source of the emboli, very little progress has been made in the pharmacological management of this high mortality condition. Because the prognosis is linked to the degree of elevation of pulmonary vascular resistance, any therapeutic intervention to improve the hemodynamics would probably increase the low survival rate of this critical condition. Inhaled nitric oxide (iNO) has been widely tested and used in cases of pulmonary hypertension of different causes. In the last few years some authors have described beneficial effects of iNO in animal models of acute PE and in anecdotal cases of massive PE. The primary cause of death in massive PE that is caused by deep venous thrombi, gas or amniotic fluid, is acute right heart failure and circulatory shock. Increased pulmonary vascular resistance following acute PE is the cumulative result of mechanical obstruction of pulmonary vessels and pulmonary arteriolar constriction (attributable to a neurogenic reflex and to the release of vasoconstrictors). As such, the vasodilator effects of iNO could actively oppose the pulmonary hypertension following PE. This hypothesis is consistently supported by experimental studies in different animal models of PE, which demonstrated that iNO decreased (by 10 to 20%) the pulmonary artery pressure without improving pulmonary gas exchange. Although maximal vasodilatory effects are probably achieved by less than 5 parts per million iNO, which is a relatively low concentration, no dose-response study has been published so far. In addition to the animal studies, a few anecdotal reports in the literature suggest that iNO may improve the hemodynamics during acute PE. However, no prospective, controlled

  8. The crosstalk between gut inflammation and gastrointestinal disorders during acute pancreatitis.

    Guo, Zhen-Zhen; Wang, Pu; Yi, Zhi-Hui; Huang, Zhi-Yin; Tang, Cheng-Wei

    2014-01-01

    The intestinal inflammation caused by intestinal ischemia reperfusion during acute pancreatitis (AP) often leads to multiple organ dysfunction and aggravation of acute pancreatitis. This review concerns up-date progress of the pathophysiology and molecular mechanism of the excessive production of gut-derived cytokines. The regulation effects of immuno-neuro-endocrine network for pancreatic necrosis are the basis for pharmacological therapeutic in AP. The translation from basic research to clinical trials for the prevention or treatment of severe acute pancreatitis (SAP) is of great value. Early enteral nutrition is necessary for the restitution, proliferation, and differentiation of the intestinal epithelial cells adjacent to the wounded area. Clearance of the excess intestinal bacteria and supplement of probiotics may be helpful to prevent bacterial translocation and infection of pancreas. PMID:23782148

  9. Neutrophil DNA contributes to the antielastase barrier during acute lung inflammation.

    Balloy, Viviane; Sallenave, Jean-Michel; Crestani, Bruno; Dehoux, Monique; Chignard, Michel

    2003-06-01

    During acute lung inflammation, the airspaces are invaded by circulating neutrophils. These may then injure tissues through the release of elastase. Different natural specific inhibitors such as alpha1-proteinase inhibitor, secretory leukocyte proteinase inhibitor, and elafin are nonetheless able to counteract the enzymatic activity of elastase. The present study was undertaken to assess the role of these different inhibitors in the intrinsic antielastase barrier during lipopolysaccharide-induced lung inflammation in mice. Upon intranasal administration of lipopolysaccharide to mice, the antielastase activity recovered from bronchoalveolar lavage fluids (BALF) increases progressively up to 48 h (7-fold) and returns to the basal level within 72 h. By contrast, when the same experiments are performed with neutropenic mice (pretreatment with an antigranulocyte antibody, or vinblastine), the increase is almost totally absent. Ultrafiltration of BALF through 100 kD cutoff membranes shows that the activity remains in the retentate, thus ruling out a role for native alpha1-proteinase inhibitor, secretory leukocyte proteinase inhibitor, and elafin. Gel filtration and fraction analysis show that the material eluted with a Mr of 600 kD. Agarose gel electrophoresis and ethidium bromide staining reveal that the activity corresponds to the presence a large amount of DNA. Interestingly, DNase treatment of the active fraction suppresses the antielastase activity. Analysis of BALF from patients with acute lung inflammation shows the presence of DNA with antielastase activity. We therefore concluded that during acute lung inflammation, the recruitment of neutrophils in the airspaces accounts for the increased presence of DNA, which in turn contributes to the antielastase barrier. PMID:12600833

  10. Review of ventilatory techniques to optimize mechanical ventilation in acute exacerbation of chronic obstructive pulmonary disease

    Reddy, Raghu M.; Guntupalli, Kalpalatha K.

    2007-01-01

    Chronic obstructive pulmonary disease (COPD) is a major global healthcare problem. Studies vary widely in the reported frequency of mechanical ventilation in acute exacerbations of COPD. Invasive intubation and mechanical ventilation may be associated with significant morbidity and mortality. A good understanding of the airway pathophysiology and lung mechanics in COPD is necessary to appropriately manage acute exacerbations and respiratory failure. The basic pathophysiology in COPD exacerbat...

  11. Systemic interleukin-2 administration improves lung function and modulates chorioamnionitis-induced pulmonary inflammation in the ovine fetus.

    Willems, Monique G M; Ophelders, Daan R M G; Nikiforou, Maria; Jellema, Reint K; Butz, Anke; Delhaas, Tammo; Kramer, Boris W; Wolfs, Tim G A M

    2016-01-01

    Chorioamnionitis, an inflammatory reaction of the fetal membranes to microbes, is an important cause of preterm birth and associated with inflammation-driven lung injury. However, inflammation in utero overcomes immaturity of the premature lung by inducing surfactant lipids and lung gas volume. Previously, we found that lipopolysaccharide (LPS)-induced chorioamnionitis resulted in pulmonary inflammation with increased effector T cells and decreased regulatory T cell (Treg) numbers. Because Tregs are crucial for immune regulation, we assessed the effects of interleukin (IL)-2-driven selective Treg expansion on the fetal lung in an ovine chorioamnionitis model. Instrumented fetuses received systemic prophylactic IL-2 treatment [118 days gestational age (dGA)] with or without subsequent exposure to intra-amniotic LPS (122 dGA). Following delivery at 129 dGA (term 147 dGA), pulmonary and systemic inflammation, morphological changes, lung gas volume, and phospholipid concentration were assessed. IL-2 pretreatment increased the FoxP3(+)/CD3(+) ratio, which was associated with reduced CD3-positive cells in the fetal lungs of LPS-exposed animals. Prophylactic IL-2 treatment did not prevent pulmonary accumulation of myeloperoxidase- and PU.1-positive cells or elevation of bronchoalveolar lavage fluid IL-8 and systemic IL-6 concentrations in LPS-exposed animals. Unexpectedly, IL-2 treatment improved fetal lung function of control lambs as indicated by increased disaturated phospholipids and improved lung gas volume. In conclusion, systemic IL-2 treatment in utero preferentially expanded Tregs and improved lung gas volume and disaturated phospholipids. These beneficial effects on lung function were maintained despite the moderate immunomodulatory effects of prophylactic IL-2 in the course of chorioamnionitis. PMID:26519206

  12. Human umbilical cord mesenchymal stem cells reduce systemic inflammation and attenuate LPS-induced acute lung injury in rats

    Li Jianjun

    2012-09-01

    Full Text Available Abstract Background Mesenchymal stem cells (MSCs possess potent immunomodulatory properties and simultaneously lack the ability to illicit immune responses. Hence, MSCs have emerged as a promising candidate for cellular therapeutics for inflammatory diseases. Within the context of this study, we investigated whether human umbilical cord-derived mesenchymal stem cells (UC-MSCs could ameliorate lipopolysaccharide- (LPS- induced acute lung injury (ALI in a rat model. Methods ALI was induced via injection of LPS. Rats were divided into three groups: (1 saline group(control, (2 LPS group, and (3 MSC + LPS group. The rats were sacrificed at 6, 24, and 48 hours after injection. Serum, bronchoalveolar lavage fluid (BALF, and lungs were collected for cytokine concentration measurements, assessment of lung injury, and histology. Results UC-MSCs increased survival rate and suppressed LPS-induced increase of serum concentrations of pro-inflammatory mediators TNF-α, IL-1β, and IL-6 without decreasing the level of anti-inflammatory cytokine IL-10. The MSC + LPS group exhibited significant improvements in lung inflammation, injury, edema, lung wet/dry ratio, protein concentration, and neutrophil counts in the BALF, as well as improved myeloperoxidase (MPO activity in the lung tissue. Furthermore, UC-MSCs decreased malondialdehyde (MDA production and increased Heme Oxygenase-1 (HO-1 protein production and activity in the lung tissue. Conclusion UC-MSCs noticeably increased the survival rate of rats suffering from LPS-induced lung injury and significantly reduced systemic and pulmonary inflammation. Promoting anti-inflammatory homeostasis and reducing oxidative stress might be the therapeutic basis of UC-MSCs.

  13. Melatonin reduces acute lung inflammation, edema,and hemorrhage in heatstroke rats

    Wen-shiann WU; Ming-ting CHOU; Chien-ming CHAO; Chen-kuei CHANG; Mao-tsun LIN; Ching-ping CHANG

    2012-01-01

    Aim:To assess the therapeutic effect of melatonin on heat-induced acute lung inflammation and injury in rats.Methods:Heatstroke was induced by exposing anesthetized rats to heat stress (36 ℃,100 min).Rats were treated with vehicle or melatonin (0.2,1,5 mg/kg) by intravenous administration 100 min after the initiatioin of heatstroke and were allowed to recover at room temperature (26 ℃).The acute lung injury was quantified by morphological examination and by determination of the volume of pleural exudates,the number of polymorphonuclear (PMN) cells,and the myeloperoxidase (MPO) activity.The concentrations of tumor necrosis factor,interleukin (IL)-1β,IL-6,and IL-10 in bronchoalveolar fluid (BALF) were measured by ELISA.Nitric oxide (NO)level was determined by Griess method.The levels of glutamate and lactate-to-pyruvate ratio were analyzed by CMA600 microdialysis analyzer.The concentrations of hydroxyl radicals were measured by a procedure based on the hydroxylation of sodium salicylates leading to the production of 2,3-dihydroxybenzoic acid (DHBA).Results:Melatonin (1 and 5 mg/kg ) significantly (i) prolonged the survival time of heartstroke rats (117 and 186 min vs 59 min); (ii)attenuated heatstroke-induced hyperthermia and hypotension; (iii) attenuated acute lung injury,including edema,neutrophil infiltration,and hemorrhage scores; (iv) down-regulated exudate volume,BALF PMN cell number,and MPO activity; (v) decreased the BALF levels of lung inflammation response cytokines like TNF-alpha,interleukin (IL)-1β,and IL-6 but further increased the level of an anti-inflammatory cytokine IL-10; (vi) reduced BALF levels of glutamate,lactate-to-pyruvate ratio,NO,2,3-DHBA,and lactate dehydrogenase.Conclusion:Melatonin may improve the outcome of heatstroke in rats by attenuating acute lung inflammation and injury.

  14. Correlation between CT features and clinical severity stratification in acute pulmonary embolism

    Objective: To analyze the correlation factors between CT imaging features of pulmonary embolism (PE) and clinical severity stratification, to explore the value of CT pulmonary angiography (CTPA) in acute PE severity stratification. Methods: According to the clinical severity, 48 patients with acute PE proved by CTPA were classified into two groups, including 21 critical and 27 non-critical patients. Embolism index, ratio of central pulmonary involvement, ratio of right ventricle maximum minor axis (RVMMA) to left ventricle maximum minor axis (LVMMA), namely RV: LV, dilation of main pulmonary and/or right pulmonary trunk, and dilation of bronchial arteries in both groups were analyzed comparatively. The correlation factors between CT imaging features and PE clinical severity stratification were explored. The correlation between RV: LV and embolism index of 48 patients was analyzed. Results: Pulmonary embolism index (22.0%-85.0%, median 38.0%), ratio of central pulmonary involvement (42.5%), RV: LV (0.90-1.90, median 1.30), dilation of pulmonary artery (14 eases), and dilation of bronchial artery (8 eases) in critical group (21 eases) were higher than those corresponding factors (5%-48%, median 21.5%, 31.25%, 0.80-1.40, median 1.00, 5 cases, and 3 cases) in non-critical group (27 cases) (Z=4.27, χ2=5.40, Z=2.58, χ2=11.45, χ2=4.87, P<0.05). There was remarkable correlation between RV: LV and embolism index (r=0.61, P<0.05). Conclusion: CTPA is feasible in evaluating PE severity stratification. The higher the embolism index, RV:LV, and the ratio of central pulmonary involvement, the higher probability of serious hemodynamic changes in PE patients. (authors)

  15. Tiotropium Attenuates Virus-Induced Pulmonary Inflammation in Cigarette Smoke-Exposed Mice.

    Bucher, Hannes; Duechs, Matthias J; Tilp, Cornelia; Jung, Birgit; Erb, Klaus J

    2016-06-01

    Viral infections trigger exacerbations in chronic obstructive pulmonary disease (COPD), and tiotropium, a M3 receptor antagonist, reduces exacerbations in patients by unknown mechanisms. In this report, we investigated whether tiotropium has anti-inflammatory effects in mice exposed to cigarette smoke (CS) and infected with influenza virus A/PR/8/34 (H1N1) or respiratory syncytial virus (RSV) and compared these effects with those of steroid fluticasone and PDE4-inhibitor roflumilast. Mice were exposed to CS; infected with H1N1 or RSV; and treated with tiotropium, fluticasone, or roflumilast. The amount of cells and cytokine levels in the airways, lung function, and viral load was determined. NCI-H292 cells were infected with H1N1 or RSV and treated with the drugs. In CS/H1N1-exposed mice, tiotropium reduced neutrophil and macrophage numbers and levels of interleukin-6 (IL-6) and interferon-γ (IFN-γ) in the airways and improved lung function. In contrast, fluticasone increased the loss of body weight; failed to reduce neutrophil or macrophage numbers; increased IL-6, KC, and tumor necrosis factor-α (TNF-α) in the lungs; and worsened lung function. Treatment with roflumilast reduced macrophage numbers, IL-6, and KC in the lungs but had no effect on neutrophil numbers or lung function. In CS/RSV-exposed mice, treatment with tiotropium, but not fluticasone or roflumilast, reduced neutrophil numbers and IL-6 and TNF-α levels in the lungs. Viral load of H1N1 and RSV was significantly elevated in CS/virus-exposed mice and NCI-H292 cells after fluticasone treatment, whereas tiotropium and roflumilast had no effect. In conclusion, tiotropium has anti-inflammatory effects on CS/virus-induced inflammation in mice that are superior to the effects of roflumilast and fluticasone. This finding might help to explain the observed reduction of exacerbation rates in COPD patients. PMID:27016458

  16. A functional variant of elafin with improved anti-inflammatory activity for pulmonary inflammation.

    Small, Donna M; Zani, Marie-Louise; Quinn, Derek J; Dallet-Choisy, Sandrine; Glasgow, Arlene M A; O'Kane, Cecilia; McAuley, Danny F; McNally, Paul; Weldon, Sinéad; Moreau, Thierry; Taggart, Clifford C

    2015-01-01

    Elafin is a serine protease inhibitor produced by epithelial and immune cells with anti-inflammatory properties. Research has shown that dysregulated protease activity may elicit proteolytic cleavage of elafin, thereby impairing the innate immune function of the protein. The aim of this study was to generate variants of elafin (GG- and QQ-elafin) that exhibit increased protease resistance while retaining the biological properties of wild-type (WT) elafin. Similar to WT-elafin, GG- and QQ-elafin variants retained antiprotease activity and susceptibility to transglutaminase-mediated fibronectin cross-linking. However, in contrast to WT-elafin, GG- and QQ-elafin displayed significantly enhanced resistance to degradation when incubated with bronchoalveolar lavage fluid from patients with cystic fibrosis. Intriguingly, both variants, particularly GG-elafin, demonstrated improved lipopolysaccharide (LPS) neutralization properties in vitro. In addition, GG-elafin showed improved anti-inflammatory activity in a mouse model of LPS-induced acute lung inflammation. Inflammatory cell infiltration into the lung was reduced in lungs of mice treated with GG-elafin, predominantly neutrophilic infiltration. A reduction in MCP-1 levels in GG-elafin treated mice compared to the LPS alone treatment group was also demonstrated. GG-elafin showed increased functionality when compared to WT-elafin and may be of future therapeutic relevance in the treatment of lung diseases characterized by a protease burden. PMID:25189740

  17. Spiral CT in the diagnosis of acute pulmonary embolism

    The traditional approach in patients with clinically suspected pulmonary embolism includes ventilation-perfusion (V/Q) scintigraphy as the first step. This relatively fast and noninvasive technique allows diagnosis or exclusion of pulmonary embolism in a considerable proportion of patients. However, depending on the patient group and evaluation criteria, the results of the V/Q lung scan are nondiagnostic in 40 to 70% of cases. Further testing is needed because pulmonary embolism will be present in only about a quarter of these patients. In order to find a non-invasive strategy for the diagnostic work-up of PE, several promising developments have been made, e.g. D-dimer analysis and spiral CT angiography. Both techniques are fast, noninvasive, and easy to perform and are now conquering the medical world. In this overview we will focus on Spiral CT: what is its role now and what might be expected in the near future? (orig.)

  18. Spiral CT in the diagnosis of acute pulmonary embolism

    Hartmann, I.J.C.; Prokop, M. [Univ. Medical Center Utrecht, Utrecht (Netherlands)

    2002-07-01

    The traditional approach in patients with clinically suspected pulmonary embolism includes ventilation-perfusion (V/Q) scintigraphy as the first step. This relatively fast and noninvasive technique allows diagnosis or exclusion of pulmonary embolism in a considerable proportion of patients. However, depending on the patient group and evaluation criteria, the results of the V/Q lung scan are nondiagnostic in 40 to 70% of cases. Further testing is needed because pulmonary embolism will be present in only about a quarter of these patients. In order to find a non-invasive strategy for the diagnostic work-up of PE, several promising developments have been made, e.g. D-dimer analysis and spiral CT angiography. Both techniques are fast, noninvasive, and easy to perform and are now conquering the medical world. In this overview we will focus on Spiral CT: what is its role now and what might be expected in the near future? (orig.)

  19. An interesting cause of pulmonary emboli: Acute carbon monoxide poisoning

    Sevinc, A.; Savli, H.; Atmaca, H. [Gaziantep University, Gaziantep (Turkey). School of Medicine

    2005-07-01

    Carbon monoxide poisoning, a public health problem of considerable significance, is a relatively frequent event today, resulting in thousands of hospitalizations annually. A 70-year-old lady was seen in the emergency department with a provisional diagnosis of carbon monoxide poisoning. The previous night, she slept in a tightly closed room heated with coal ember. She was found unconscious in the morning with poor ventilation. She had a rare presentation of popliteal vein thrombosis, pulmonary emboli, and possible tissue necrosis with carbon monoxide poisoning. Oxygen treatment with low-molecular-weight heparin (nadroparine) and warfarin therapy resulted in an improvement in both popliteal and pulmonary circulations. In conclusion, the presence of pulmonary emboli should be sought in patients with carbon monoxide poisoning.

  20. A PAF receptor antagonist inhibits acute airway inflammation and late-phase responses but not chronic airway inflammation and hyperresponsiveness in a primate model of asthma

    R. H. Gundel

    1992-01-01

    Full Text Available We have examined the effects of a PAF receptor antagonist, WEB 2170, on several indices of acute and chronic airway inflammation and associated changes in lung function in a primate model of allergic asthma. A single oral administration WEB 2170 provided dose related inhibition of the release of leukotriene C4 (LTC4 and prostaglandin D2 (PGD2 recovered and quantified in bronchoalveolar lavage (BAL fluid obtained during the acute phase response to inhaled antigen. In addition, oral WEB 2170 treatment in dual responder primates blocked the acute influx of neutrophils into the airways as well as the associated late-phase airway obstruction occurring 6 h after antigen inhalation. In contrast, a multiple dosing regime with WEB 2170 (once a day for 7 consecutive days failed to reduce the chronic airway inflammation (eosinophilic and associated airway hyperresponsiveness to inhaled methacholine that is characteristic of dual responder monkeys. Thus, we conclude that the generation of PAF following antigen inhalation contributes to the development of lipid mediators, acute airway inflammation and associated late-phase airway obstruction in dual responder primates; however, PAF does not play a significant role in the maintenance of chronic airway inflammation and associated airway hyperresponsiveness in this primate model.

  1. Acute exacerbations of chronic obstructive pulmonary disease provide a unique opportunity to take care of patients

    Bianca Beghé

    2013-04-01

    Full Text Available Exacerbation of chronic obstructive pulmonary disease (ECOPD identifies the acute phase of COPD. The COPD patient is often frail and elderly with concomitant chronic diseases. This requires the physician not only looks at specific symptoms or organs, but to consider the patient in all his or her complexity.

  2. Pathmorphological investigation of pulmonary infections complications in persons dying from acute radiation sickness after Chernobyl accident

    Lungs of 27 persons who participated in liquidation of Chernobyl accident and died from acute radiation sickness were studied histologically. Pulmonary infections were found, including invasion of viral, bacterial and fungal agents. Being depended on hematopoietic function the inflammatory reactions were areactive during postirradiation aplasia and became typical within the recovery beginning

  3. Distinguishing the Causes of Pulmonary Infiltrates in Patients With Acute Leukemia.

    Nucci, Marcio; Nouér, Simone A; Anaissie, Elias

    2015-06-01

    Pulmonary infiltrates are commonly observed in patients with acute leukemia (AL), particularly acute myeloid leukemia, who undergo remission induction therapy. The mortality rate is unacceptably high and depends on 3 factors: the host (performance status, comorbidities, and frailty), the etiology of the infiltrates and the type of response to antileukemic therapy. The approach to the diagnosis of pulmonary infiltrates in patients with AL includes a medical history, thorough physical examination, radiologic pattern of the infiltrates (focal vs. diffuse), and timing of their appearance in relation to the start of antileukemic therapy (early, ie, within the first 2 weeks or late). Localized infiltrates are most commonly caused by bacterial (early) and fungal infections (late). Diffuse early infiltrates might be caused by leukemic infiltration of the lungs, pulmonary hemorrhage and/or edema, diffuse alveolar damage, viral pneumonia, and rarely transfusion-related acute lung injury (TRALI) or the differentiation syndrome. Similar to the early phase, pulmonary edema, viral pneumonia, and rarely TRALI might cause diffuse infiltrates during the late phase, in addition to immune reconstitution and pneumocystosis, particularly among patients with acute lymphoblastic leukemia. Diagnostic tests, invasive and noninvasive, can be particularly useful to establish the diagnosis. Early intervention is critical and is based on the most likely diagnosis with modification when the etiology is confirmed. PMID:26297289

  4. Bacteriology in acute exacerbation of chronic obstructive pulmonary disease in patients admitted to hospital

    Larsen, Mette V; Janner, Julie H; Nielsen, Susanne D; Friis-Møller, Alice; Ringbaek, Thomas; Lange, Peter

    2009-01-01

    We investigated the bacterial flora and antimicrobial sensitivity in sputum from patients admitted to hospital with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) in order to recommend the best empirical treatment for these patients. The survey was a retrospective study of a...... AECOPD we recommend either cefuroxime for intravenous treatment or amoxicillin-clavulanate for oral treatment....

  5. Clinical and radiological characterization of the pulmonary commitment for acute toxoplasmosis disseminated in nine immunocompetent patients

    The acute toxoplasmosis in the immunocompetent individual generally has a benign and autoresolutive course. However, in patient coming from wild area severe cases of visceral commitment, the most frequent in them, the pulmonary commitment has been reported. The clinical and radiological description of nine individuals members of the military forces of Colombia, with acute toxoplasmosis and pulmonary commitment was carried. 55% of the cases presented dysnea functional class II/IV; 33% functional class III/IV and only 1/9 patients presented functional class IV/IV. The most common radiological image was the uni focal or multifocal consolidation pulmonary (66%), and in smaller frequency the presence of having infiltrated reticular, reticulo nodular and pleural effusion. The entirety of the patients evolved in satisfactory form, two of them with support with noninvasive ventilation.

  6. An alteration of the gut-liver axis drives pulmonary inflammation after intoxication and burn injury in mice.

    Chen, Michael M; Zahs, Anita; Brown, Mary M; Ramirez, Luis; Turner, Jerrold R; Choudhry, Mashkoor A; Kovacs, Elizabeth J

    2014-10-01

    Approximately half of all adult burn patients are intoxicated at the time of their injury and have worse clinical outcomes than those without prior alcohol exposure. This study tested the hypothesis that intoxication alters the gut-liver axis, leading to increased pulmonary inflammation mediated by burn-induced IL-6 in the liver. C57BL/6 mice were given 1.2 g/kg ethanol 30 min prior to a 15% total body surface area burn. To restore gut barrier function, the specific myosin light chain kinase inhibitor membrane-permeant inhibitor of kinase (PIK), which we have demonstrated to reduce bacterial translocation from the gut, was administered 30 min after injury. Limiting bacterial translocation with PIK attenuated hepatic damage as measured by a 47% reduction in serum alanine aminotransferase (P intoxicated and burn-injured mice without PIK. This mitigation of hepatic damage was associated with a 49% decline in pulmonary neutrophil infiltration (P antibiotics before intoxication and burn injury. Overall, these data suggest that the gut-liver axis is deranged when intoxication precedes burn injury and that limiting bacterial translocation in this setting attenuates hepatic damage and pulmonary inflammation. PMID:25104501

  7. Oxidative stress–induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease

    Wiegman, Coen H.; Michaeloudes, Charalambos; Haji, Gulammehdi; Narang, Priyanka; Clarke, Colin J.; Russell, Kirsty E.; Bao, Wuping; Pavlidis, Stelios; Barnes, Peter J.; Kanerva, Justin; Bittner, Anton; Rao, Navin; Murphy, Michael P.; Kirkham, Paul A.; Chung, Kian Fan; Adcock, Ian M.; Brightling, Christopher E.; Davies, Donna E.; Finch, Donna K.; Fisher, Andrew J.; Gaw, Alasdair; Knox, Alan J.; Mayer, Ruth J.; Polkey, Michael; Salmon, Michael; Singh, David

    2015-01-01

    Background Inflammation and oxidative stress play critical roles in patients with chronic obstructive pulmonary disease (COPD). Mitochondrial oxidative stress might be involved in driving the oxidative stress–induced pathology. Objective We sought to determine the effects of oxidative stress on mitochondrial function in the pathophysiology of airway inflammation in ozone-exposed mice and human airway smooth muscle (ASM) cells. Methods Mice were exposed to ozone, and lung inflammation, airway hyperresponsiveness (AHR), and mitochondrial function were determined. Human ASM cells were isolated from bronchial biopsy specimens from healthy subjects, smokers, and patients with COPD. Inflammation and mitochondrial function in mice and human ASM cells were measured with and without the presence of the mitochondria-targeted antioxidant MitoQ. Results Mice exposed to ozone, a source of oxidative stress, had lung inflammation and AHR associated with mitochondrial dysfunction and reflected by decreased mitochondrial membrane potential (ΔΨm), increased mitochondrial oxidative stress, and reduced mitochondrial complex I, III, and V expression. Reversal of mitochondrial dysfunction by the mitochondria-targeted antioxidant MitoQ reduced inflammation and AHR. ASM cells from patients with COPD have reduced ΔΨm, adenosine triphosphate content, complex expression, basal and maximum respiration levels, and respiratory reserve capacity compared with those from healthy control subjects, whereas mitochondrial reactive oxygen species (ROS) levels were increased. Healthy smokers were intermediate between healthy nonsmokers and patients with COPD. Hydrogen peroxide induced mitochondrial dysfunction in ASM cells from healthy subjects. MitoQ and Tiron inhibited TGF-β–induced ASM cell proliferation and CXCL8 release. Conclusions Mitochondrial dysfunction in patients with COPD is associated with excessive mitochondrial ROS levels, which contribute to enhanced inflammation and cell

  8. Dioscin alleviates dimethylnitrosamine-induced acute liver injury through regulating apoptosis, oxidative stress and inflammation.

    Zhang, Weixin; Yin, Lianhong; Tao, Xufeng; Xu, Lina; Zheng, Lingli; Han, Xu; Xu, Youwei; Wang, Changyuan; Peng, Jinyong

    2016-07-01

    In our previous study, the effects of dioscin against alcohol-, carbon tetrachloride- and acetaminophen-induced liver damage have been found. However, the activity of it against dimethylnitrosamine (DMN)-induced acute liver injury remained unknown. In the present study, dioscin markedly decreased serum ALT and AST levels, significantly increased the levels of SOD, GSH-Px, GSH, and decreased the levels of MDA, iNOS and NO. Mechanism study showed that dioscin significantly decreased the expression levels of IL-1β, IL-6, TNF-α, IκBα, p50 and p65 through regulating TLR4/MyD88 pathway to rehabilitate inflammation. In addition, dioscin markedly up-regulated the expression levels of SIRT1, HO-1, NQO1, GST and GCLM through increasing nuclear translocation of Nrf2 against oxidative stress. Furthermore, dioscin significantly decreased the expression levels of FasL, Fas, p53, Bak, Caspase-3/9, and upregulated Bcl-2 level through decreasing IRF9 level against apoptosis. In conclusion, dioscin showed protective effect against DMN-induced acute liver injury via ameliorating apoptosis, oxidative stress and inflammation, which should be developed as a new candidate for the treatment of acute liver injury in the future. PMID:27317992

  9. Modified PISAPED Criteria in Combination with Ventilation Scintigraphic Finding for Predicting Acute Pulmonary Embolism.

    Watanabe, Naoyuki; Fettich, Jure; Küçük, Nurie Özlem; Kraft, Otakar; Mut, Fernando; Choudhury, Partha; Sharma, Surendra K; Endo, Keigo; Dondi, Maurizio

    2015-01-01

    This prospective clinical study aimed at assessing three pulmonary scintigraphic algorithms to detect acute pulmonary embolism (PE): Lung ventilation/perfusion (V/Q) scintigraphy along with modified prospective investigation of pulmonary embolism diagnosis (PIOPED) criteria; lung perfusion scintigraphy along with prospective investigative study of acute pulmonary embolism diagnosis (PISAPED) criteria; and lung perfusion scan in combination with ventilation scan, along with modified PISAPED criteria, which were newly developed. Patients with suspicion of PE were eligible for this study if they had no abnormal chest x-ray. Their diagnostic workup included a clinical assessment, a pulmonary V/Q scintigraphy, and CT pulmonary angiography (CTPA), as well as a clinical outcome assessment over a period of 24 weeks. Referred to the final clinical diagnosis of patients, the sensitivity and specificity of each algorithm were evaluated. The diagnostic performance of each algorithm by the area under the maximum likelihood fitted receiver operating characteristic (ROC) curve was determined. With respect to the PISAPED criteria, the sensitivity was 60.8% and specificity was 87.3%. No patient was classified into nondiagnostic category. The PIOPED criteria showed that the sensitivity was 95.0% and specificity was 88.2%, while 57.4% of the patients were in nondiagnostic category. The areas under the ROC curve constructed from the PISAPED criteria results and the modified PIOPED criteria results were 0.734 and 0.859 (P < 0.01), respectively. The modified PISAPED criteria demonstrated that the sensitivity was 83.8% and specificity was 89.1%. No patient was classified into nondiagnostic category. The area under the ROC curve constructed from modified PISAPED criteria was 0.864 (P < 0.01). Perfusion scans used with ventilation scans and modified PISAPED criteria may increase the diagnostic accuracy of pulmonary scintigraphy for acute PE, compared with the two major algorithms. PMID

  10. Establishment and evaluation of acute pulmonary embolism model in rabbit monitored with echocardiography

    Objective: To establish acute pulmonary embolism (APE) model in rabbit under echocardiography, and compare with the pathological results, and explore the feasibility of establishment of APE model monitored with echocardiography. Methods: APE models were established in 25 healthy Japanese white rabbits. The rabbit models of APE were created by right external jugular vena catheter using gelatin sponge monitored with echocardiography. Gelatin sponge emboli, 2 mm x 2 mm x 10 mm each, following with 5 mL physiologic saline were injected separately to right atrium via the right external jugular vein, which could make these emboli embolize pulmonary artery following blood stream. And the pulmonary artery systolic pressure was detected. Then the lung tissues slices near embolism place were detected by pathology after the model rabbits were dissected. Results: Twenty-three rabbit models with APE were successfully established from twenty-five healthy rabbits. However, one rabbit was unexpectedly dead because of anesthesia, another rabbit was dead owing to acute congestive heart failure of cor dextrum by emboli stagnation in cor dextrum. The echocardiogram of rabbits before and after model establishment showed that the pulmonary artery systolic pressure was significantly increased after APE, the main pulmonary artery, the left pulmonary artery and the right pulmonary artery were passively expanded. The right ventricle was increased and left ventricle was decreased oppositely, interventricular septum expanded toward left ventricle. there was significant difference compared with pre-embolism (P< 0.01). Gelatin sponge emboli in the pulmonary artery were detected by pathological detection. Conclusion: The method to establish APE model monitored with echocardiography is simple and feasible. It could be used as one of methods to establish APE model, animal. (authors)