Inhibition of PGI2 (prostacyclin) synthesis in the arterial wall enhances the formation of white platelet thrombi in vivo.

Prostaglandins play an important role in platelet-vessel wall interactions. Cyclic endoperoxides PGG2 and PGH2 are transformed to PGI2 (prostacyclin) within the arterial wall. The inhibition of PGI2 synthetase results in a marked enhancement of white platelet thrombus formations. This finding suggests that the synthesis of PGI2 from PGG2 and PGH2 accounts for the nonthrombogenicity of the endothelium.