Cardiovascular effects of prostaglandin D3 and D2 in anesthetized dogs

Prostaglandin (PG) D3 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 microgram/kg) of PGD3 and also PGD2 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 PGD3. A biphasic (depressor followed by a pressor phase) effect on systemic arterial pressure was observed after PGD2, while PGD3 was associated with dose-related depressor responses. Graded intravenous infusions (0.25, 0.50 and 1.0 microgram/kg/min) of PGD3 and PGd2 were associated with qualitatively similar cardiovascular responses. Quantitatively, PGD3 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 PGD2. In contrast, PGD3 was less potent than PGD2 as a pulmonary pressor material. Systemic arterial pressure responses to infusions of the prostaglandins were variable. In these experiments, PGD3 and PGD2 were associated with qualitatively similar cardiovascular responses characterized by peripheral vasodilatation.