No abstract

This paper summarizes the evidence in favor of the theory that many of the platelet’s factors are adsorbed onto its surface from the plasma. It is suggested that this ability of the platelet is one of its basic functions. The platelet adsorbs coagulation and perhaps vascular factors on its surface and carries them through the circulation to the area where they are needed most—at the site of vessel wall injury. This adsorption by the platelet may be an active rather than a passive process, since it requires the expenditure of energy and since it continues only so long as the platelet is viable. In those diseases in which there is marked abnormality of the plasma proteins, there is evidence to suggest that associated coagulation and hemostatic defects may be due to interference with this "atmosphère plasmatique."

Since chloramphenicol is an efficient broad spectrum antibiotic that is widely used, the possibility that it may be the cause of hematological disorders is, naturally, a serious one. Recently, five cases of fatal aplastic anemia have come to our attention. In each instance, we believe chloramphenicol to be etiologically implicated. It

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.