Excitation-contraction coupling in heart. XII. Subcellular calcium transport in isoproterenol-induced myocardial necrosis

Calcium transport by cardiac subcellular particles in isoproterenol-induced myocardial necrosis in rats and rabbits was investigated. The ability of mitochondria to bind and accumulate calcium in the necrotic heart was similar to that of the control. Calcium binding, but not calcium uptake, by heavy microsomes of the necrotic heart was found to be depressed. This change in calcium was apparent over a wide pH range as well as at various concentrations of calcium in the incubation medium. The decrease in calcium binding by heavy microsomes was not due to the efflux of calcium from the microsomal vesicles and was seen within 1 hr of the subcutaneous injection of isoproterenol. At an increased animal room ambient temperature, not only was mortality due to isoproterenol injection increased, but also a decrease in the calcium uptake by heavy microsomes of the surviving animals was observed. These results suggest an alteration in the regulatory mechanisms responsible for the control of intracellular calcium in the necrotic heart.