It is thought that platelets have a major role in maintaining vascular integrity as in conditions where their number and function is abnormal, widespread capillary haemorrhages occur. In health, platelets are constantly sealing microdefects. Minifibrin clots are formed, and the fibrin is then removed by the fibrinolytic system. Prostacyclin (PGI2) is an unstable compound, first discovered in 1976. It is the principal prostanoid synthesised by blood vessels and is a potent vasodilator and inhibitor of platelet aggregation. It is proposed that there is a balance between prostacyclin and thromboxane A2 — a powerful vasoconstrictor and platelet aggregating agent. Prostacyclin prevents aggregation at much lower concentrations than is needed to prevent adhesion. Therefore, vascular damage leads to platelet adhesion, but not necessarily platelet aggregation and thrombus formation. If injury is small, small platelet thrombi form and are washed away by the circulation. The extent of the injury is, however, an important determinant of the size of the thrombus and whether or not platelet aggregation is stimulated. PGI2 syntethase is abundant in the intima and progressively decreases from the intima to the adventitia. It follows that severe vessel damage or physical detachment of the endothelium will lead to development of a large thrombus rather than simple platelet adherence.
An essential function of the haemostatic system is rapid reaction to injury, which remains confined to the area of damage. Control mechanisms are required to stimulate coagulation after trauma and limit the extent of the response. The substances involved in the formation of the haemostatic plug normally circulate in inert form until activated at the site of injury or by some factor released in the circulation that will trigger off intravascular coagulation.
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