Abstract
Trauma to blood vessels or degenerative changes in atherosclerotic plaques result in exposure of structures in the subendothelium, such as collagen, which in its native state is stimulatory for platelet adhesion and subsequent activation (Marcus, 1988). Platelet activation is also accompanied by initiation of the blood coagulation cascade, culminating in the formation of thrombin. Collagen and thrombin are capable of stimulating the oxygenation of free arachidonate, thereby activating the eicosanoid pathway in both platelets and endothelial cells. Many of the eicosanoids which form are actually autacoids with significant biological properties.
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