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Platelet function in atherosclerosis is briefly reviewed. Although there was controversy whether atherosclerosis is activated by changing of blood platelet function accompanied by an increasing of hyperlipidemia.
Mustard and his co-worker had suggested since 1969 & 1972 that
platelets play an important part in development of some forms of atherosclerosis and occlusive thrombi. However the response to injury hypothesis of atherogenesis have provided an approach to exploring the interactions between blood platelets with both overlying and underlying endothelial cells. This in turn would release substances from each of these cells, which play a role in the induction of the proliferative response. The proliferated vascular smooth muscle cells and lipids accumulation would, a period of months or years, lead to the development of fibrous plaque, the advanced lesion of atherosclerosis. Meanwhile it may be superimposed by some vasoactive molecules, prostanoids, such as activation of thromboxane A2 synthesized by blood platelets and inhibition of prostacyclin by vascular endothelium.
The studies of current status of platelets in atherosclerosis and the potential role of some vasoactive prostanoids in generating occlusive lesions have begun to throw light on the approaching to the new trends in the effective treatment and prevention of atherosclerosis and thromboembolic conditions.
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