Prostaglandin I2 (PG I2) fails to inhibit ADP induced platelet aggregation in vivo in rats.
There is a simple method of inducing cardiopulmonary dysfunction in rats through platelet aggregation after rapid i.v. administration of ADP and thrombin. Infusion of 25 ng/min/kg PGI2 completely inhibited the decrease of both breathing and heart rate induced by 30 IU/kg thrombin. The same PGI2 infusion failed to influence the cardiopulmonary effects of the different ADP doses (between 75 and 0.1 mg/kg). Some possible reasons for the differential effectiveness of PGI2 are discussed on the basis of the modes of action of ADP, thrombin, and PGI2. The results stress the necessity of testing antiaggregatory substances in in vivo models.
D000244:Adenosine Diphosphate / Q000494:pharmacology*; D000818:Animals; D011464:Epoprostenol / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D012119:Respiration / Q000187:drug effects; D013917:Thrombin / Q000494:pharmacology
D000244:Adenosine Diphosphate; D011464:Epoprostenol; D013917:Thrombin