A protective effect of verapamil on hypoxic heart muscle.

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 incolves 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 aerobie (pO2 greater than 80.0 kPa [600 mm Hg]) or hypoxie (pO2 less than 0.80 kPa [6 mmHg]) conditions, and either with or without glucose substrate, 0.5-1.0 mg/litre dl verapamil reduced the amount of ultrastructural damage caused by hypoxie perfusion. Verapamil (0.5-1.0 mg/litre) also reduced the rate at which the hypoxie muscle gained Na+ and lost K+; it reduced the rate at which the endogenous stores of ATP and CP were depleted and, provided that the extracellular phase contained Ca2+, it decreased the rate at which CPK appeared in the coronary effluent. Verapamil failed to prevent the hypoxie muscle from gaining Ca2+. These results are discussed in terms of a possible protective effect of dl verapamil on hypoxie heart muscle.