Vessel injury, platelet adherence, and platelet survival.

T relationship among platelet survival, vessel injury, and thrombosis is of interest because of the role that platelets play in the development of atherosclerosis and its thromboembolic complications. Blood platelets do not adhere to normal endothelium. However, when a blood vessel is injured, platelets adhere to the injury site and, if blood flow is disturbed, thrombi can form on the injured area. In arteries, fresh thrombi are composed largely of aggregated platelets and are stabilized by fibrin, whereas in veins, although thrombi may be initiated by a mass of aggregated platelets in a valve pocket, the thrombi are mainly composed of red blood cells in a fibrin network. In large normal arteries that have not been previously injured in which blood flow is laminar, only a thin layer of platelets coats the subendothelium when the endothelium is lost. If flow is disturbed, for example at vessel orifices and branches, so that platelets are brought into close contact with each other, thrombus formation will occur because of the accumulation of aggregating agents released from the platelets and thrombin that is generated at the injury site. Thrombi are not static structures, but have been shown to undergo episodic formation and dissolution. Several processes contribute to the dissolution of thrombi. These include the force of flowing blood, platelet deaggregation, and lysis of fibrin. Theoretically, if injury to blood vessels is extensive or repeated, resulting in consumption of a significant proportion of the circulating platelets, a reduction in platelet survival would be expected. Thus, it is not surprising that vessel wall injury is a common feature of many conditions in which platelet survival is shortened (table 1). Although there are