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Previous studies have shown that after autonomic blockade by propranolol and atropine, the intrinsic rate and contractile function of the heart were related in patients with myocardial failure. In this study the intrinsic rate and ventricular contractile force were measured in dogs during acute heart failure produced by agents which impair myocardial energy syntinesis, to see whether these conditions reproduced the relationship found in naturally occurring myocardial disease in man. Anesthetized dogs, after propranolol and atropine, were either ventilated with 6% oxygen or given sodium cyanide, parachloromercuribenzoate, or dinitrophenol by intravenous infusion. Hypoxia and cyanide initially increased and then depressed both rate and contraction. Parachloromercuribenzoate depressed both. Dinitrophenol depressed only contraction. During hypoxia, cyanide, and parachloromercuribenzoate the percent changes in contractile force and intrinsic rate were linearly related (r=0.87) with slopes of 3.2, 2.7, and 3.3, respectively. These results together with previous data during pentobarbital and aminophylline were consistent with a single linear relationship between rate and contractility (r=0.89, slope 3.2). This resembled closely the relationship found previously in man. It is suggested that in both situations, this relationship may be determined by a dependence of rate and contractility on similar limited sources of energy.

Effects of Hypoxia and Metabolic Inhibitors on the Intrinsic Heart Rate and Myocardial Contractility in Dogs