Key result
Intravenous prostacyclin inhibits thrombus formation and platelet aggregation while increasing bleeding time.
Why the study?
The effects of prostacyclin on platelet behavior, thrombus formation in vivo, and bleeding time were investigated to understand its potency compared to other prostaglandins.
May support short-acting PGI2 analogs for thrombosis; leaves open translation to human cardiovascular therapy.
Summary 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.
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Ubatuba et al. (1979) studied this question. Prostacyclin (PGI2) vs. Prostaglandin E1 (PGE1) or prostaglandin D2 (PGD2) was evaluated on Electrically-induced thrombus formation, bleeding time, and ex vivo platelet aggregation. Prostacyclin (PGI2) infused intravenously into anaesthetized rabbits inhibited electrically-induced thrombus formation and platelet aggregation, and increased bleeding time.
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