Abstract
The contribution of hemodynamic changes to the pathogenesis of accelerated fibrinolysis in liver disease was investigated in rats. In animals with hepatic lesions induced by a 7-week inhalation of carbon tetrachloride there was a significant increase in blood t-PA activity and PAI activity, with no significant change in portal pressure. Following a 10-min portal vein occlusion there was a marked increase in portal pressure and t-PA activity and a significant decrease in PAI activity. Following ligation of both portal vein and hepatic artery, t-PA activity increased to a higher extent and PAI activity was reduced to a lesser extent than changes found in portalstenosed rats. Our data suggest that high t-PA circulating levels in liver disease could be related not only to the reduced t-PA clearance as a consequence of liver injury but also to hemodynamic changes.
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