Abstract

These studies were performed to examine the effects of 6-keto-prostaglandin E1 (6-keto-PGE1) on coronary artery blood flow and reflex cardiovascular regulation. In seven chloralose-anesthetized dogs 6-keto-PGE1 and prostacyclin (PGI2) were injected as a bolus into the left circumflex coronary artery in doses of 250 to 4000 ng. Coronary artery blood flow significantly increased and coronary artery resistance decreased in a dose-related manner. There were no significant differences observed between 6-keto-PGE1 and PGI2 in the magnitude of the maximum increase in coronary blood flow or decrease in coronary artery resistance. In six additional anesthetized dogs in which the carotid arteries were ligated in order to minimize baroreflexes, intracoronary injection of 6-keto-PGE1 and PGI2 (in doses of 7, 14 and 23 micrograms) caused systemic hypotension and bradycardia. Bilateral vagotomy attenuated the hypotension and abolished the bradycardia induced by these substances. In five conscious dogs, 6-keto-PGE1 and PGI2 were infused (2, 10 and 20 micrograms/min i.v.) for 10 min. 6-keto-PGE1 and PGI2 caused significant decreases in mean arterial pressure; however PGI2 was significantly more potent in this respect. The tachycardia to the highest doses was compared to that induced by infusion of nitroprusside (500 micrograms/min i.v.). 6-keto-PGE1 and PGI2 caused significantly less baroreflex tachycardia per millimeter of mercury decrease in arterial pressure than did nitroprusside. Thus, in anesthetized dogs, 6-keto-PGE1 and PGI2 are equipotent coronary vasodilators. These PGs also stimulate a vagal reflex which results in hypotension, bradycardia and attenuation of baroreflex-mediated tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)