Cardiovascular effects of prostaglandin D 3 and D 2 in anesthetized dogs

Abstract

Prostaglandin (PG) D 3 has been identified as an inhibitor of human platelet aggregation, but little is known of the hemodynamic activity of this material. In morphine pretreated, chloralose-urethan anesthetized dogs, bolus intravenous injections (1, 3.2 and 10 μg/kg) of PGD 3 and also PGD 2 were associated with marked, dose-related increases in pulmonary arterial pressure. Cardiac index and rate increased, while peripheral vascular resistance decreased in response to injections of PGD 3. A biphasic (depressor followed by a pressor phase) effect on systemic arterial pressure was observed after PGD 2, while PGD 3 was associated with dose-related depressor responses. Graded intravenous infusions (0.25, 0.50 and 1.0 μg/kg/min) of PGD 3 and PGD 2 were associated with qualitatively similar cardiovascular responses. Quantitatively, PGD 3 infusions were associated with greater decreases in peripheral vascular resistance and greater increases in cardiac output, heart rate, and peak left ventricular dp/dt than were infusions of PGD 2. In contrast, PGD 3 was less potent than PGD 2 as a pulmonary pressor material. Systemic arterial pressure responses to infusions of the prostaglandins were variable. In these experiments, PGD 3 and PGD 2 were associated with qualitatively similar cardiovascular responses characterized by peripheral vasodilatation.