COAGULATION in vivo is a dynamic process; the concurrent formation and lysis of clots maintains the blood fluid. Human plasma contains an inactive proteolytic enzyme precursor called plasminogen.1,2 When it is activated by the various kinases, plasmin (fibrinolysin) is formed. Plasmin acts upon fibrin, fibrinogen, plasma factors V and VII, and produces soluble split products, thus affecting the formation or the already formed blood clots. There are two inhibitors in the plasminogen system: one is activator inhibitor and the other is antiplasmin. Normally the activators and the inhibitors are in a state of equilibrium, preventing the generation of abnormal fibrinolytic activity. This equilibrium may be disrupted temporarily by liberation of plasminogen activators as in anoxia, shock, surgical trauma, anxiety, etc,1-3 and the ensuing increase in fibrinolytic activity can interfere with the hemostatic process.4
The purpose of this investigation is to establish the relationship between fibrinolytic activity and