Platelet physiology—facts and fiction

The formation of prostaglandins and thromboxanes by platelets is one of several mechanisms which contribute to the basic platelet function, formation of an hemostatic plug. Following vessel injury in normal subjects, platelet adhesion to exposed, connective tissue, release of ADP from platelets and damaged red cells, stimulation of thrombin generation, and conversion of platelet membrane arachidonate into prostaglandins, all contribute to platelet aggregation and plug formation. Thus, only minor prolongation of the bleeding time is produced by aspirin and other prostaglandin synthesis inhibitors. On the other hand, hemostatic plug formation is more strongly dependent on platelet prostaglandin formation when thrombin formation is defective as in patients with hemophilia, and particularly when both platelet adhesion to connective tissue and thrombin formation are defective as in patients with Bon Willebrand's disease. In these diseases, aspirin produces serious prolongation of bleeding times. The initial evidence that the formation of prostacyclin by the vessel wall acts to prolong hemostasis has not been substantiated at this time.