The effect of prostacyclin (PGT2) on platelet behaviour. Thrombus formation in vivo and bleeding time.
Prostacyclin (PGI2) infused intravenously into anaesthetized rabbits inhibited electrically-induced thrombus formation in the carotid artery, increased bleeding time and inhibited ex vivo platelet aggregation induced by ADP or arachidonic acid. The increase in bleeding time and the inhibition of ex vivo platelet aggregation lasted for as long as the infusion of PGI2 was maintained but rapidly disappeared after infusion was stopped. Prostacyclin is a more potent inhibitor of platelet function, in vivo than prostaglandin E1 (PGE1) or prostaglandin D2 (PGD2). The effects of prostacyclin on all parameters studied except blood pressure were potentiated by the concomitant administration of theophylline, a phosphodiesterase inhibitor.
D000818:Animals; D001777:Blood Coagulation; D001780:Blood Coagulation Tests; D001794:Blood Pressure; D002339:Carotid Arteries / Q000473:pathology; D004558:Electric Stimulation; D011464:Epoprostenol / Q000494:pharmacology*; D005260:Female; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology*; D011457:Prostaglandins D / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology; D011817:Rabbits; D013806:Theophylline / Q000494:pharmacology
D011453:Prostaglandins; D011457:Prostaglandins D; D011458:Prostaglandins E; D013806:Theophylline; D011464:Epoprostenol