1. Platelet and fibrinogen survival have been studied by isotope tagging in normal and abnormal states of coagulation in humans and dogs.
2. By our technic, the normal curve of platelet survival is exponential. Evidence is given that such a curve is obtained because of random utilization of the platelets in the continuous process of coagulation.
3. In the postoperative subject and in the subject receiving epinephrine injections, platelet survival is shortened because the process of coagulation is speeded up. In the hypocoagulable, the curve of platelet survival becomes more nearly linear because random platelet destruction ceases.
4. When a massive thrombus forms, platelet survival is shortened. Evidence is given that this may be due to escape of thrombin from the clot into the systemic circulation—with a resultant hypercoagulable state.
5. Fibrinogen survival was not altered in those states in which increased platelet utilization occurred. This is explained by the theory that the alteration in the hemostatic mechanism had not penetrated to the fibrinogen-fibrin stage.
6. Hypercoagulability is defined as that state in which platelet utilization is accelerated—whether or not thrombosis occurs.