Electrophysiological effects of ethanol, acetaldehyde, and acetate on cardiac tissues from dog and guinea pig.

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Abstract
Superfusion of isolated canine cardiac Purkinje fibers with ethanol (100-300 mg/100 ml) resulted in a concentration-dependent shortening of action potential duration. The effect occurred within 5 min of exposure to ethanol and was reversed completely after removal of the drug from the medium. Action potential amplitude, transmembrane resting potential, dV/dt [1st derivative of left ventricular pressure] of phase 0 and conduction time were not altered by these concentrations of ethanol. Superfusion with methanol, ethanol, t-butanol, n-butanol and pentanol in a concentration of 200 mg/100 ml, revealed that the magnitude of the alcohol-associated shortening of action potential duration was related directly to the water-octanol partition coefficient (lipophilic property) of the alcohol. Acetaldehyde (0.08-0.80 mM) prolonged the action potential duration of Purkinje fibers, but this effect was blocked by addition of the .alpha.-adrenergic blocking drug, phentolamine (10-6 M). Acetate (1-5 mM) did not alter action potential configuration or conduction time of cardiac Purkinje fibers. Ethanol (100-300 mg/100 ml), acetaldehyde (0.08-0.80 mM) and acetate (1-5 mM) did not significantly change the rate of spontaneous depolarization of isolated guinea pig atria. Ethanol, in concentrations present in plasma during ethanol consumption, exerts direct reversible effects on cardiac Purkinje fibers. These effects probably result from a physical alteration of the sarcolemma secondary to interaction of ethanol with hydrophobic regions of the lipid bilayer. The metabolic byproducts of ethanol do not exert direct electrophysiological effects on canine Purkinje fibers or guinea pig atria.