ROIIELL, TIMOTHY C., JOHN C. CHERONIS, CHRISTZEL. OHNEMUS,DALEJ.PIERMATTEI, JOHN E. REPINE.X~W thine mediates elastase-induced to isolated s endothelium. J. Appl. Physiol. 63(5): 21594163, 1987. (X8) -generated toxic O2 metabolites appear to contribute to reperfusion , but the possibility that X0 is involved in hyperoxic or neutrophil elastase-mediated has not been investigated. We found that s isolated from rats fed a tungsten-rich diet had negligible X0 activities after exposure to hyperoxia developed less edematous during perfusion with buffer or purified neutrophil elastase than X0-replete s from control rats which had been exposed to hyperoxia. In parallel, tungsten-treated XO-depleted cultured bovine pulmonary arterial endothelial cells made less superoxide anion as monolayers leaked less lz51labeled albumin after exposure to neutrophil elastase than XOreplete endothelial cell monolayers. Our findings suggest that X0-derived O2 metabolites contribute to edematous from hyperoxia directly by enhancing susceptibility to neutrophil elastase. endothelial cells; edema; hyperoxia; neutrophil elastase oxygen metabolites; TOXIC OXYGEN METABOLITES have been implicated in the development of edematous , such as that seen in pulmonary O2 toxicity the adult respiratory distress syndrome (ARDS) (7,17). The sources of O2 metabolites in from hyperoxia are unknown but may be from the accelerated oxidative metabolism of pulmonary parenchymal
Journal of Applied Physiology – The American Physiological Society
Published: Nov 1, 1987
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