Changes of the fibrinolytic system in liver dysfunction: role of portal hypertension.
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 portal-stenosed 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.
Lasierra
J
J
Department of Hematology, San Millán Hospital, Logroño, Spain.
Barrao
F
F
Ceña
G
G
Aza
M J
MJ
Morandeira
M J
MJ
Barrao
M E
ME
González-Gallego
J
J
D000595:Amino Acid Sequence; D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000097:blood; D005342:Fibrinolysis; D006439:Hemodynamics; D006975:Hypertension, Portal / Q000097:blood*; D008026:Ligation; D008106:Liver Cirrhosis, Experimental / Q000097:blood* / Q000139:chemically induced; D008297:Male; D008969:Molecular Sequence Data; D010634:Phenobarbital / Q000633:toxicity; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis*; D051381:Rats; D017208:Rats, Wistar; D010959:Tissue Plasminogen Activator / Q000032:analysis*
D017395:Plasminogen Activator Inhibitor 1; D010959:Tissue Plasminogen Activator; D010634:Phenobarbital