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IDELL, STEVEN, KATHLEEN B. KOENIG, DARYL S. FAIR, THOMAS R. MARTIN, JERRY MCLARTY, AND RICHARD J. MAUNDER. abnormalities of in evolving adult respiratory distress syndrome. Am. J. Physiol. 261 (Lung Cell. Mol. Physiol. 5): L240-L248, 1991.-We studied the changes of coagulation and olysis in bronchoalveolar (BAL) and plasma obtained ly at intervals after the onset of adult respiratory distress syndrome (). BAL procoagulant activity was increased at 3 days and tended to decrease thereafter. Tissue factor associated with factor VII was the major BAL procoagulant. opeptide A was increased, indicating increased thrombin-mediated conversion of ogen to . olytic activity was usually undetectable in BAL at 3 days post- and remained depressed for up to 14 days despite unchanged concentrations of urokinase and variably detectable tissue plasminogen activator. Depressed olytic activity was associated with increased antiplasmin activity and plasminogen activator inhibitor 1 (PAI-1) while PAIconcentrations approximated those of control samples and did not change during evolving . Evidence of systemic coagulopathy and increased systemic degradation were commonly found in plasma samples, consistent with accelerated vascular and/or extravascular deposition in these patients. The data indicate that intra-alveolar as well as systemic derangements of are common features of evolving . Concurrent
AJP - Lung Cellular and Molecular Physiology – The American Physiological Society
Published: Oct 1, 1991
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