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Stranica 1 iz 93 rezultatima
Inhibition of neutrophil elastase attenuates gut mucosal injury evoked by acute alveolar hypoxia in rabbits.
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The aim of the present study was to examine whether neutrophil and its elastase activity played consequential roles in the progression of gut barrier dysfunction during acute alveolar hypoxia by using a specific neutrophil elastase inhibitor, sivelestat. With our institutional approval, 20 male
Anoxia-reoxygenation-induced, neutrophil-mediated endothelial cell injury: role of elastase.
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The aim of this study was to assess the role of neutrophilic elastase in anoxia-reoxygenation-induced, neutrophil-mediated injury to microvascular endothelium. Cultured bovine microvascular endothelial cells were grown to confluence and labeled with 51Cr. The endothelial cells were exposed to a
Hypoxia sensitization of hepatocytes to neutrophil elastase-mediated cell death depends on MAPKs and HIF-1α.
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The liver is sensitive to pathological conditions associated with tissue hypoxia (Hx) and the presence of activated neutrophils that secrete the serine protease elastase (EL). We demonstrated previously that cotreatment of rat hepatocytes with nontoxic levels of Hx and EL caused synergistic cell
The effect of oxygen on Cor pulmonale in experimental emphysema induced by elastase or elastase and beta-aminopropionitrile in hamsters.
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Right ventricular hypertrophy in elastase-induced emphysema in the System hamster was assessed by either the weight of the right ventricle as a fraction of body-weight or by the ratio of the weight of the right to the left ventricle. Right ventricular hypertrophy accompanies elastase-induced
Neutrophil elastase, von Willebrand factor, soluble thrombomodulin and percutaneous oxygen in peripheral atherosclerosis.
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OBJECTIVE
To test the hypothesis that endothelial cell damage and hypoxia are related to the activity of neutrophil elastase in patients with peripheral atherosclerosis.
METHODS
A cross-sectional serological study in a tertiary referral, University Hospital.
METHODS
Venous blood was obtained from 22
Leukocyte elastase inhibition and t-PA-induced coronary artery thrombolysis in dogs: beneficial effects on myocardial histology.
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Leukocyte-derived elastase is released following coronary artery occlusion and reperfusion and may contribute to reperfusion-related myocardial injury. Leukocyte infiltration into the reperfused myocardium may also contribute to ischemic injury following reflow. In the present study, we examined the
The effects of nitric oxide and peroxynitrite on interleukin-8 and elastase from lipopolysaccharide-stimulated whole blood.
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Inhaled nitric oxide is now widely used in the treatment of hypoxemia and pulmonary hypertension in critically ill patients. Interleukin-8 (IL-8) and neutrophil elastase are important markers of the onset and severity of acute lung injury. We studied the effects of nitric oxide and peroxynitrite on
Temporal changes in mouse aortic wall gene expression during the development of elastase-induced abdominal aortic aneurysms.
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OBJECTIVE
To characterize temporal changes in mouse aortic wall gene expression associated with the development of experimental abdominal aortic aneurysms.
METHODS
C57BL/6 mice underwent transient perfusion of the abdominal aorta with either elastase (n = 61) or heat-inactivated elastase as a
Microvascular permeability of the non-heart-beating rabbit lung after warm ischemia and reperfusion: role of neutrophil elastase.
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BACKGROUND
The duration of warm ischemia and reperfusion injury is a major limiting factor in the setting of lung transplantation with non-heart-beating donors (NHBD). We hypothesized that reperfusion with neutrophil elastase inhibitor or leukocyte-depleted blood has an inhibitory effect on the
[Case of acute respiratory distress syndrome in which high-frequency oscillatory ventilation (HFOV) was effective for the management of severe hypoxemia].
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A 69-year-old man was admitted to our hospital because of acute prostatitis. After admission he produced bloody sputum and chest radiograph showed bilateral infiltration of the upper lung fields. The fraction of neutrophils in the bronchoalveolar lavage fluid was 15.6%, lymphocytes were 33.6%,
Coagulation-mediated hypoxia and neutrophil-dependent hepatic injury in rats given lipopolysaccharide and ranitidine.
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Idiosyncrasy-like liver injury occurs in rats cotreated with nonhepatotoxic doses of ranitidine (RAN) and bacterial lipopolysaccharide (LPS). Hepatocellular oncotic necrosis is accompanied by neutrophil (PMN) accumulation and fibrin deposition in LPS/RAN-treated rats, but the contribution of PMNs to
Pulmonary haemodynamics in awake rats following treatment with endotracheal pancreatic elastase.
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The purpose of this paper was to study pulmonary haemodynamics in an elastase-induced emphysema model in awake rats (Group-EL, n = 9) in comparison with saline-treated controls (Group-C, n = 12). Four weeks before haemodynamic study, porcine pancreatic elastase and normal saline were intratracheally
Growth and protease secretion of Scedosporium aurantiacum under conditions of hypoxia.
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One of the micro-environmental stresses that fungal pathogens, such as Scedosporium aurantiacum, colonising human lungs encounter in vivo is hypoxia, or deficiency of oxygen. In this work, we studied the impacts of a hypoxic micro-environment (oxygen levels ≤1%) on the growth of a clinical S.
Cytotoxic response of sinusoidal endothelial cells to polymorphonuclear leukocytes and its potential implication in hypoxia-reoxygenation injury.
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OBJECTIVE
Interactions between polymorphonuclear leukocytes (PMN) and sinusoidal endothelial cells (SEC) may contribute to ischemia-reperfusion injury. The aim of the study was to determine the influence of PMN hypoxia-reoxygenation and degranulation, on SEC toxic response.
METHODS
PMNs collected
Hypoxia suppresses elastin repair by rat lung fibroblasts.
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Macrophage and neutrophil proteinases damage lung elastin, disrupting alveolar epithelium and filling alveoli with inflammatory exudate. Alveolar collapse and regional hypoxia occur. Whether low oxygen tension alters fibroblast-mediated lung repair is unknown. To determine the effect of chronic
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