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Effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema in the rat.
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The effect of a synthetic leukocyte elastase inhibitor on thrombin-induced pulmonary edema was studied in rats. The chloromethylketone human neutrophil elastase inhibitor, ICI 200,355, blunted rat leukocyte elastase activity in rat lung tissue. Administration of thrombin produced a significant
Using a Caesalpinia echinata Lam. protease inhibitor as a tool for studying the roles of neutrophil elastase, cathepsin G and proteinase 3 in pulmonary edema.
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Acute lung injury (ALI) is characterized by neutrophil infiltration and the release of proteases, mainly elastase (NE), cathepsin G (Cat G) and proteinase 3 (PR3), which can be controlled by specific endogenous inhibitors. However, inhibitors of these proteases have been isolated from different
Prevention of Pulmonary Edema after Minimally Invasive Cardiac Surgery with Mini-Thoracotomy Using Neutrophil Elastase Inhibitor.
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OBJECTIVE
Unilateral re-expansion pulmonary edema (RPE) is a rare but one of the most critical complications that may occur after re-expansion of a collapsed lung after minimally invasive cardiac surgery (MICS) with mini-thoracotomy.
METHODS
We performed a total of 40 consecutive patients with MICS
Effect of a selective neutrophil elastase inhibitor on mortality and ventilator-free days in patients with increased extravascular lung water: a post hoc analysis of the PiCCO Pulmonary Edema Study.
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BACKGROUND
Neutrophil elastase plays an important role in the development and progression of acute respiratory distress syndrome (ARDS). Although the selective elastase inhibitor, sivelestat, is widely used in Japan for treating ARDS patients, its effectiveness remains controversial. The aim of the
Neutrophil elastase inhibitor prevents ischemic brain damage via reduction of vasogenic edema.
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Release of neutrophil elastase is one of the harmful inflammatory reactions in acute cerebral ischemia. Therefore, inhibition of elastase released from neutrophils could be a useful strategy for the treatment of acute stroke. To evaluate this hypothesis, the effect of sivelestat, a selective
Influence of the lysosomal elastase inhibitor eglin on the development of interstitial lung edema in E. coli bacteremia in pigs.
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Infusion of 3 X 10(10) live E. coli cells into anesthetized piglets induced severe septicemia with characteristic alterations in systemic and pulmonary circulation, lung function and morphology, blood cell counts and plasma protein composition. The simultaneous infusion of the elastase-cathepsin G
Involvement of lung interstitial proteoglycans in development of hydraulic- and elastase-induced edema.
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We extracted and isolated proteoglycans from lung tissue samples obtained from three groups of anesthetized rabbits: 1) control animals (C; n = 8) killed by overdose after 180 min; 2) animals receiving an intravenous saline infusion (S; n = 4, 1.5 ml . kg-1 . min-1) for 180 min; 3) animals receiving
Interstitial pressure and proteoglycan degradation in hydraulic- and elastase-induced lung edema.
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Inhibition of neutrophil elastase contributes to attenuation of lipopolysaccharide-induced acute lung injury during neutropenia recovery in mice.
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OBJECTIVE
Patients in whom neutropenia recovery is complicated by pneumonia have an increased risk of acute lung injury (ALI) and detrimental outcomes. The aim of the present study was to investigate whether inhibition of neutrophil elastase (NE) is effective in lipopolysaccharide (LPS)-induced ALI
Inhibition of elastase-induced acute inflammation and pulmonary emphysema in hamsters by a novel neutrophil elastase inhibitor FR901277.
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OBJECTIVE
A neutrophil elastase inhibitor FR901277 was examined for its inhibitory effect on degradation of natural substrate elastin in vitro, and on acute inflammatory states and pulmonary emphysema in vivo.
METHODS
Elastin-congo red was used as a substrate for elastin degradation assay. Paw edema
Ultrastructural studies of elastase-induced experimental emphysema.
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Experimental emphysema in the guinea pig was made by intracheal instillation of porcine pancreatic elastase in order to analyze the proteolytic factors related to the pathogenesis of pulmonary emphysema. Ultrastructural and morphometric studies were performed in the elastase-induced emphysema in
Biochemical and pharmacological characterization of FR134043, a novel elastase inhibitor.
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FR134043, disodium(Z,1S,15S,8S,24S,27R,29S,34S,37R)-29-ben zyl-21-ethylidene-27-hydroxy-15-isobutyrylamino-34-isopropyl-31,37 -dimethyl-10,16,19,22,30,32,35,38-octaoxo-36-oxa-9,11,17,20,23,28, 31,33-octaazatetracyclo[16.13.6.1(24),(28).0(3),(8)]octatricont a-3,5,7-trien-5,6-diyl disulfate, is a
Morphological and biochemical features of elastase-induced emphysema in strain A/J mice.
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Elastase-induced animal models of pulmonary emphysema are potentially useful to study the physiological, anatomical, and biochemical injuries associated with emphysema. After the endotracheal instillation of porcine pancreatic elastase (0.15 or 0.30 mg elastase per 100 g body weight) into strain A/J
Differing susceptibility of young and adult hamster lungs to injury with pancreatic elastase.
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A study was undertaken to determine whether there are differences in the initial response of the lungs of young (28 days) and adult (105 days) hamsters to pancreatic elastase treatment. The elastase was given intratracheally (0.1 mg/100 g body weight), and the animals were studied 24 h later. The
Physiologic and morphologic observations of the effects of intravenous elastase on the lung.
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Intravenous administration of porcine pancreatic elastase to hamsters produced significant loss of elastic recoil at low volumes. Histology and mean linear intercept of the lungs fixed at a pressure of 20 cm H2O and studied for 3 weeks after administration of elastase were normal. Larger doses of
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