Platelets serve two main functions: (1) to protect intact blood vessels from endothelial damage provoked by the countless microtraumas of day-to-day existence and (2) to initiate repair through the formation of platelet plugs when blood vessel walls are damaged.
When overt trauma or microtrauma damages blood vessels, platelets adhere to the altered surface. Adherence requires the presence of ionized calcium (coagulation factor IV), fibrinogen (coagulation factor I), and a protein associated with coagulation factor VIII, called von Willebrand's factor (vWF). The process of adherence involves reversible changes in platelet shape and, usually, the release of adenosine diphosphate (ADP), adenosine triphosphate (ATP), calcium, and serotonin. With a strong enough stimulus, the next phase of platelet activity, platelet aggregation, occurs and results in the formation of a loose plug in the damaged endothelium. The platelet plug aids in controlling bleeding until a blood clot has had time to form.1
Platelets generate prostaglandins that ultimately promote platelet adherence, whereas the endothelial cells lining the blood vessels produce a different prostaglandin that inhibits platelet aggregation. Ingestion of aspirin inhibits the actions of the prostaglandins released by platelets, an effect that may persist for many days after a person takes even a small amount of aspirin. Aspirin also may affect the actions of the prostaglandins produced by endothelial cells, but not to the extent that it affects platelet prostaglandins.2 Thus, the net effect of aspirin is to inhibit hemostasis.
Thrombin, which is generated by the coagulation sequence (see the next section), independently promotes the release of substances from the platelets. Release of platelet factor 3 enhances coagulation mechanisms, thereby increasing thrombin generation. Platelet factor 4, also released by platelets, reinforces the interactions between coagulation and platelet aggregation by neutralizing the naturally generated anticoagulant, endogenous heparin.3