Abstract

When nicotinic acid was given intraperitoneally to rats, there was a marked decrease in the ventricular force of contraction and in the inotropic response to 1-norepinephrine at 2 and 4 hours after administration of the drug; 6 hours after the injection of nicotinic acid, myocardial contractility had returned to normal. Severe impairment in cardiac contractility coincided with the period when heart triglycerides and myocardial glycogen were depleted by the nicotinic acid. Inclusion of oleic acid, triglyceride, or glucose in the medium perfusing the heart restored normal contractility and the inotropic response to 1-norepinephrine. Results of these experiments indicate a direct relationship between myocardial contractility and the availability of energy-supplying substrates.

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