A protective effect of verapamil on hypoxic heart muscle

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Abstract
Hypoxic-induced damage of rabbit heart muscle has been quantitated in terms of the release of intracellular enzymes (including creating phosphokinase, CPK) into the extracellular space, a gain in tissue Na+ and Ca2+, a loss of tissue K+, the depletion of the adenosine triphosphate (ATP) and creatine phosphate (CP) reserves, and ultrastructural damage. This ultrastructural damage involves the disruption of the plasmalemma, swelling and distortion of the mitochondria, disruption of the myofilaments, and the development of contraction bands. In isolated Langendorff-perfused rabbit hearts perfused under either aerobic (pO2>80.0 kPa [600 mm Hg]) or hypoxic (pO2 2+, it decreased the rate at which CPK appeared in the coronary effluent. Verapamil failed to prevent the hypoxic muscle from gaining Ca2+. These results are discussed in terms of a possible protective effect of dl verapamil on hypoxic heart muscle.