“…Exogenous PGI2 can partially inhibit the binding of platelets to newly exposed areas of the subendothelium (1,3,27,28). There is, however, conflicting data concerning whether inhibition, of vascular PGI2 production by nonsteroidal antiinflammatory agents enhances platelet adherence to newly deendothelialized areas of arterial walls (29)(30)(31)(32). Nevertheless, after a damaged artery begins to repair itself, there is an increase in the capacity bf the deendothelialized vessel to form PGI2 from arachidonic acid that correlates with the formation of a nonthrombogenic neointimal surface (26).…”