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Abstract
Carboprostacyclin, a chemically stable analogue of prostacyclin (PGI 2) is 12.5 and 25.0 times respectively weaker than PGI 2 in inhibiting ADP-induced aggregation of baboon and human platelets in vitro. Carboprostacyclin was also 28.5 times weaker as a vasodepressor than PGI 2 in anaesthetised baboons. Intravenous and oral administration of carboprostacyclin in baboons resulted in ex-vivo inhibition of ADP-induced platelet aggregation at doses that did not produce changes in blood pressure or heart rate. Like PGI 2, carboprostacyclin contracted guinea pig tracheal chain preparation in vitro but decreased histamine induced lung resistance in anaesthetised guinea pigs. Both PGI2 and carboprostacyclin relaxed the human respiratory tract smooth muscle in vitro.
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