Considerations of Platelet Function Mechanisms

Abstract

Physiological haemostasis and pathological thrombosis are both initiated by platelet aggregation, and the involvement of platelets in both processes is more evident in arteries than in veins. Thrombosis in coronary arteries begins on sites damaged by atherosclerosis. Commonly a thrombus grows on an atherosclerotic plaque which has narrowed the lumen. With the blood pressure constant the blood flow is faster in the constricted lumen than elsewhere in the artery. Therefore, high flow and shear rates are no hindrance to thrombogenesis where the thrombus consists essentially of adhering and aggregating platelets. Indeed, the question arises whether the activation of platelets required for thrombus formation depends in some Way on such abnormal haemodynamic conditions. When adequately anticoagulated blood is made to flow under conditions giving rise to flow separation or vortices, e.g., in artificial dialysers or oxygenators, platelets are deposited on the channel walls to form obstructive thrombi. Measurements of the haemodynamic forces required to activate platelets directly (Hellums & Brown, 1977) indicate that the flow abnormalities caused by atherosclerotic lesions in vivo cannot account for local activation of circulating platelets.