Effects of prostaglandin E1 and 15-methyl-prostaglandin E1 on the cardiovascular responses to bilateral carotid arterial occlusion

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Abstract
Intravenous administration of prostaglandin E1 (PGE1), and 15-methyl-prostaglandin E1 (15-CH3-PGE1) caused a progressive fall in systemic arterial pressure. The haemodynamic responses such as tachycardia, hypertension, and increased dp/dt due to bilateral carotid arterial occlusion were progressively decreased or abolished along with the depressor effect of these prostaglandins. As systemic arterial pressure returned to control levels following the administration of angiotensin II or vasopressin, the haemodynamic responses to carotid occlusion were restored. This study indicates that the homeostatic cardiovascular reflex mechanism is markedly impaired during continuous intravenous infusion of PGE1 or following a single intravenous injection of 15-CH3-PGE1. This may be due not only to the inhibitory action of the prostaglandins on norepinephrine release from sympathetic nerve endings but also to their marked vasodilator action per se.

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