Relationship of insulin and strophanthidin to myocardial metabolism and function

¹ Department of Medicine, Seton Hall College of medicine, Thomas J. White Cardiopulmonary Institute, and B. S. Pollak Hospital for Chest Diseases, Jersey City, New Jersey
² Department of Medicine, Seton Hall College of Medicine, Thomas J. White Cardiopulmonary Institute, and B. S. Pollak Hospital for Chest Diseases, Jersey City, New Jersey

The relevance of changes in substrate and ion transport to left ventricular contractility alterations have been examined after insulin, strophanthidin, and their combination, using serial arterial-coronary sinus differences in intact anesthetized dogs. Insulin (0.1 U/kg) was infused into a left coronary artery catheter to minimize systemic changes, producing an accumulated left ventricular uptake of glucose, lactate, and potassium with a rise in respiratory quotient, without affecting pyruvate and free fatty acid extractions. There was no associated change in the dp/dt_max. of left ventricular pressure or in the duration of isometric contraction, used as indices of contractility. Acetyl strophanthidin, .03 mg/kg, produced a 60% increase in dp/dt_max. and significantly shortened isometric duration associated with egress of potassium from the myocardium. Insulin, given 25 min before strophanthidin to reduce K⁺ egress, failed to do so, but largely interfered with its contractile properties. This effect was also observed with p-chloromercuribenzoate, so that a SH-binding site would seem essential for the inotropic activity of strophanthidin.

Key Words: insulin and cardiac contractility • insulin and substrate • transport in heart • carbohydrate usage and cardiac contractility • K⁺ egress and strophanthidin inotropism • cardiac K⁺ transport after insulin and strophanthidin • sulfhydryl binding and strophanthidin's inotropic effect • cardiac Qo₂ after insulin • cardiac Qo₂ after strophanthidin

Submitted on March 6, 1963

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