| Abstract: | ABSTRACT— Aims/Background: In patients with severe liver disease, blood levels of many coagulation and fibrinolytic factors are lowered due to a diminished synthetic capability in the liver. Tissue plasminogen activator (t-PA) is synthesized by the vascular endothelial cells, however, and is increased in such patients. Methods: Amounts of t-PA secreted were determined by immunosorbent assay after plasma from patients with cirrhosis was added to cultured human umbilical vein endothelial cells to determine whether a plasma factor directly enhanced t-PA secretion from vascular endothelial cells. Results: Release of t-PA was significantly higher with exposure to plasma from patients with decompensated cirrhosis than when plasma from patients with compensated cirrhosis or normal subjects was used (p<0.01 and p<0.05, respectively). Plasminogen activator inhibitor 1(PAI-1) concentrations were measured similarly but did not differ among the three groups. Conclusions: Our results indicate that factors in plasma from patients with decompensated cirrhosis directly stimulate t-PA release from the vascular endothelial cells, while any increased PAI-1 release observed in comparable in vivo situations is probably an indirect response to an increase of t-PA or a result of impaired hepatic clearance. |
