In vivo effects of ethanol on the rat myocardium: evidence for a reversible, non-specific increase of sarcolemmal permeability.

Weight paired (approximately 200 g) Long-Evans male rats (n = 48) were divided into two groups: an ethanol-consuming (A) and a water-consuming control (C) group. Ethanol concentration was raised incrementally over a one month period until it reached 25% (v/v). The diet of group C was regulated calorically to minimize differences between the two groups in the consumption of protein, fat, and carbohydrate. Half the members of each group were killed 12 weeks after initiating the special diets for the determination of myocardial electrolyte and water distributions and uptake of a tracer normally restricted to the extracellular space (ECS). The remaining rats were returned to a normal diet (recovery groups AR and CR) and killed 8 weeks later. Left ventricular tissue and plasma were analyzed for Na, K, Ca, and Mg; ECS was assessed in the same samples by tracer distribution and morphometric methods. Comparison of the myocardial [35S]sulfate space as a function of equilibration duration in the four groups indicates that the tracer leaks into the cellular compartment of alcoholic rats, suggesting that myocardial sarcolemmal permeability is increased in alcoholism. This interpretation is supported by the finding that all cations studied either were (Na, Ca) or tended to be (K, Mg) displaced down their respective electrochemical gradients. It is concluded that a reversible, non-selective sarcolemmal leakiness may be one of the earliest effects of alcoholism on the heart, eventually resulting in a redistribution of myocardial electrolytes and associated alterations of electrical, metabolic, and contractile activities.