CARDIOVASCULAR EFFECTS OF PROSTAGLANDIN E₁

¹ Department of Pharmacology, University of Oklahoma School of Medicine, Oklahoma City, Oklahoma

The cardiovascular effects of prostaglandin E₁ (PGE₁) were studied in anesthetized dogs. It was found that the i.v. administration of 0.25 to 4.0 µg/kg of PGE1 decreased arterial pressure, left atrial pressure and left ventricular end-diastolic pressure, whereas heart rate, pulmonary arterial pressure, cardiac output and myocardial contractile force increased. Right atrial pressure remained essentially unchanged. The magnitude of the hemodynamic changes observed was essentially in proportion to the dose given. In addition, PGE₁ increased significantly the maximum rate of isometric tension rise (dp/dt). It was also found that the i.a. administration of 0.1 µg/kg of PGE1 increased blood flows markedly and decreased peripheral resistances in the brachial, femoral, carotid, and renal arteries without any significant change in mean systemic arterial pressure and myocardial contractile force. Furthermore, the i.a. injection of PGE₁ caused significant increases in both coronary arterial blood flow and myocardial contractile force without any change in mean systemic arterial pressure. The i.v. injection of 1 mg/kg of propranolol, which blocked completely the positive inotropic and chronotropic actions of norepinephrine (0.5 µg/kg) and the vasodilator action of isoproterenol (0.2 µg/kg) in vagotomized dogs, did not block the positive inotropic and vasodilator actions of PGE₁ (4 µg/kg). The present study indicates that PGE₁ induces multiple hemodynamic effects primarily through its potent direct vasodilator action on all peripheral vascular beds and indirectly through reflex sympathetic stimulation. In addition, PGE₁ exerts a positive inotropic action on the heart. PGE₁, in the doses given, does not appear to block the hemodynamic effects of norepinephrine in vagotomized dogs.