Abstract
At the acute phase of cerebral thrombosis, endothelin-1 (ET-1), a vasopressor factor derived from vascula : endothelial cells, decreases with time. On the other band, tissue plasminogen activator (t-PA), a rate-determining factor of fibrinolysis, increases enantiomorphically. Elucidation of the mechanism involved is important for analyzing and for determining the guidelines for the treatment of the disease. In the present study, in an attempt to analyze the above mechanism, we conducted a basic clinical study. Release of both factors was not altered by the addition of sodium ozagrel or thrombin to cultured vascular endothelial cells. From this finding, it is denied that therapeutic drugs and coagulation may be associated with an increse in free PAI-1 which reflects the activity of PAI. In combination with previously reported results showing a decrease in the release of ET-1 following addition of t-PA, the data suggest that t-PA may influence an inhibitory effect on fibrinolysis when both factors change at the acute phase. It is considered that the increased t-PA may inhibit predominantly the relcase of ET-1 and induce resistance against thrombosis at the acute phase. In the treatment of cerebral thrombosis, we should therefore consider not only antiplatelet effects and anticoagulation but also such increase in t-PA.
