Changes in urokinase-type plasminogen activator in orthotopic liver transplantation

Elevated levels of u-PA Ag and scu-PA preoperatively and before revascularization of the graft are explained by an impaired clearance function by the diseased liver. They are parallel preoperatively and in the beginning of OLT by increased tcu-PA activity. This may reflect a role of the intrinsic fibrinolytic system in the "hyperfibrinolytic state" observed in patients with end stage liver disease. u-PA Ag and scu-PA normalize following reperfusion. The increase in tcu-PA observed during the anhepatic phase coincided with greatly increased fibrinolysis, as demonstrated by thrombelastography. This indicates that u-PA seems to be involved in the development of fibrinolysis during OLT. It had been demonstrated in previous investigations that a significant increase of t-PA activity was seen in the late anhepatic phase leading to an elevated plasmin generation. Since plasmin is a major activator of scu-PA, a t-PA mediated scu-PA activation would explain the concomitant increase in both plasminogen activators.