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.
D000818:Animals; D001158:Arteries; D001777:Blood Coagulation; D001792:Blood Platelets; D016861:Cyclooxygenase Inhibitors; D011464:Epoprostenol / Q000096:biosynthesis*; D008297:Male; D011453:Prostaglandins / Q000096:biosynthesis*; D011462:Prostaglandins G / Q000378:metabolism; D011463:Prostaglandins H / Q000378:metabolism; D051381:Rats
D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; D011462:Prostaglandins G; D011463:Prostaglandins H; D011464:Epoprostenol