RT Journal Article
SR Electronic
T1 PROSTAGLANDIN INHIBITION OF METABOLICALLY INDUCED CORONARY VASODILATION
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 135
OP 147
VO 188
IS 1
A1 F. A. Sunahara
A1 J. Talesnik
YR 1974
UL http://jpet.aspetjournals.org/content/188/1/135.abstract
AB In the isolated perfused heart, the heart activity was measured from the left ventricular pressure, dP/dt, heart rate, coronary flow and O2 tension of coronary outflow. The administration of norepinephrine, isoproterenol and dimethylphenylpiperazinium resulted in a metabolically induced increase in coronary flow (MCD). Infusion of prostaglandin E1 (PGE1) at the rate of 2.5 µg/min caused an increase in coronary flow; when the infusion rate was subsequently lowered (0.25-0.5 µg/min), the flow returned to within preinfusion range. The effects of the stimulating agents on the cardiac activities were not altered by the PGE1 infusion but the consequent MCD was greatly reduced. During this period, in comparison to pre-PGE1 infusion, cardiac stimulation showed a prolonged and larger arterial-venous PO2 difference. On the other hand, PGE1 did not alter the response to direct-acting coronary vasodilators. Thus, the inhibitory response of PGE1 is different from those described for beta adrenotropic receptor blocking agents. These studies support the view that the inhibition of the metabolically induced coronary vasodilation following increased cardiac activity by PGE1 can produce a dissociation of the coronary response from the myocardial requirements, suggesting that this autocoid may play an important role as a modulator of the feedback system that adapts the coronary flow to changing metabolic demands of the myocardium. © 1974 by The Williams & Wilkins Company