General and Local Factors in Arterial Thrombosis: Platelets, Prostaglandins and Postulates
The discovery by Moneada et al., (1976) that vessel fragments could convert prostaglandin endoperoxide G2 in an unstable metabolite with a potent antiaggregating as well as vasodilating property appeared to be a major step in the understanding of arterial thrombosis. The fact that this substance was mainly produced in the endothelial cells of the vessel wall (Moneada et al., 1977) seemed to be an additional explanation to the non thrombogenicity of the endothelium. These discoveries were followed by the emergence of the concept of antagonistic substances, namely platelet thromboxane (TX) A2 and vascular prostaglandin (PG) I2 playing a key role in the thrombocyte-vessel wall interactions. According to this concept, a balance might exist between TXA2 and PGI2 for the homeostatic regulation of platelet-vessel wall interactions. This very tempting hypothesis has stimulated a tremendous effort in the cardiovascular field, aimed at the verification of this theory as a likely explanation of most thrombotic disorders. However, at the present time, it appears that the TXA2 “ PGI2 axis may only be one part of the mediators that play a role in vascular disorders. Plasma factors, membrane components, blood cells other than platelets... may be involved in those processes.
KeywordsPlatelet Adhesion Arterial Thrombosis Eicosatetraenoic Acid Bovine Endothelial Cell Platelet Thromboxane
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