Abstract
Traces of thrombin were removed from purified preparations of autoprothrombin II-A. This thrombin-free protein, when infused intravenously into a dog, retarded blood coagulation, stopped autoprothrombin III (Factor X) utilization, and induced plasmin activity. There were no associated changes in heart rate, respiratory rate or blood pressure. In experiments with purified components, it was found that autoprothrombin II-A possessed only weak ability to directly activate either bovine or canine plasminogen to plasmin, but did depress the function of plasmin inhibitors. Autoprothrombin II-A thus induced fibrinolysis by an indirect mechanism. There is clearly a pathway from the coagulation system to fibrinolysis. Autoprothrombin II-A retarded the activity of soybean trypsin inhibitor.
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