Postcountershock Myocardial Damage after Pretreatment with Adrenergic and Calcium Channel Antagonists in Halothane-anesthetized Dogs

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Abstract
Transthoracic electric countershock can cause necrotic myocardial lesions in humans as well as experimental animals. The effect was studied on postcountershock myocardial damage of pretreatment with prazosin (0.1 mg/kg), an .alpha.-1-antagonist; L-metoprolol (0.5 mg/kg), a .beta.-1 antagonist and verapamil (0.5 mg/kg), a Ca channel-blocking agent. Twenty dogs were anesthetized with halothane and given 2 transthoracic countershocks of 295 delivered joules each after drug or vehicle treatment. Myocardial injury was quantitated 24 h following countershock by measuring the uptake of technetium-99m pyrophosphate in the myocardium. Elevated technetium-99m pyrophosphate uptake occurred in visible lesions in most dogs regardless of drug treatment. For each of 4 parameters of myocardial damage there was no statistically significant difference between control animals and those treated with prazosin, metoprolol, or verapamil. These data suggest that adrenergic or Ca channel-mediated mechanisms are not involved in the pathogenesis of postcountershock myocardial damage.