Peritoneal fibrinolysis: evidence for the efficiency of the tissue-type plasminogen activator.

Blood shed into a closed peritoneal cavity is incoagulable. We have investigated this poorly understood phenomenon in animal experiments. Nonthrombogenic femoral vein-peritoneal cavity shunts were established in five dogs and 10 ml/kg blood admixed with 125I-dog fibrinogen was rapidly drained into the peritoneal cavity. After 1 hr the peritoneal cavity was entered and incoagulable blood aspirated; 125I-fibrinogen Mr distribution was assessed by AGPC, demonstrating complete degradation of fibrinogen into core fragments D and E with no evidence of soluble fibrin complexes or crosslinked fibrin fragments. Peritoneal cavity clotting factors II, V, and VIII and platelets were sharply reduced compared to venous control samples. Plasminogen and antiplasmin levels in peritoneal cavity blood showed mean declines of 17% and 15%, respectively. By comparison, incubation of dog blood with 1 to 2 X 10(3) U/ml urokinase for 1 hr in vitro was insufficient to degrade 125I-dog fibrinogen to core fragments D and E, although plasminogen and antiplasmin were reduced by 66% and 100%, respectively. Pretreatment of dogs with epsilon ACA (0.13 gm/kg, N = 4) resulted in massive intraperitoneal cavity clotting, and aspirated fluid blood contained only small quantities of radiolabel. Heparin treatment (300 U/kg bolus, 150 U/kg/hr infusion; N = 4) eliminated the peritoneal cavity lytic response; analytical gel permeation chromatography consistently demonstrated intact fibrinogen only. Therefore it is apparent that blood in a closed peritoneal cavity undergoes limited clotting followed by brisk plasmin-mediated fibrinolysis as opposed to fibrinogenolysis. The closed peritoneal cavity fibrinolytic response to clotting blood represents a striking example of the efficiency of the "tissue-type" plasminogen activator.