SOME DIRECT AND REFLEX CARDIOVASCULAR ACTIONS OF PROSTACYCLIN (PGI2) AND PROSTAGLANDIN E2 IN ANAESTHETIZED DOGS

Abstract

1 The aim of the study was to determine the mechanism of the hypotension and bradycardia produced by prostacyclin (PGI₂). 2 Haemodynamic studies were carried out in nineteen open-chest beagle dogs anaesthetized with chloralose. PGI₂ was infused intravenously or into the left atrium. 3 Infusions of PGI₂ either intravenously or into the left atrium equally reduced arterial pressure and total peripheral resistance but bradycardia was greater after infusion into the left atrium. 4 Comparison of effects of PGI₂ with those of prostaglandin E₂ (PGE₂) showed that although left atrial infusions both reduced aortic pressure and total peripheral resistance, PGE₂ always increased heart rate, cardiac output and maximum acceleration. 5 Similar effects were observed with sodium nitroprusside except that it always caused tachycardia and reduced stroke volume. 6 Atropine (0.05 or 1 mg/kg i.v.) reduced or reversed the bradycardia induced by PGI₂ but its hypotensive effects were reduced only after 1 mg/kg atropine. After vagotomy changes in cardiac output, stroke volume and maximum acceleration were increased, the hypotensive effects of PGI₂ were reduced and the bradycardia was reversed; effects induced by PGE₂ were not significantly altered. 7 The hypotension induced by prostacyclin is due to two components, a direct relaxation of vascular smooth muscle and a reflex, non-cholinergic vasodilatation. The bradycardia is reflex in nature and is partially mediated by the vagus pathway.