An Ionic Shift Through Which Non- Specific Stimuli Can Increase the Resistance of the Heart Muscle

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Abstract
Experiments in the rat indicate that exposure to forced muscular exercise, cold baths, food deprivation, and to acute hemorrhage, possesses a common ability to protect against diverse potentially cardiotoxic influences. Under such conditions the animals become largely resistant to combined Na-acetate plus fluorocortisol administration and to the cardiac-necrosis-eliciting effect of subsequent restraint; to plasmocid, a metabolic-inhibitor compound that produces necrotizing myocarditis; and even to high doses of methoxamine, a synthetic amine with sustained pressor and vasoconstrictor potencies that invariably result in the development of ischemic infarction of the heart muscle. Studies on the electrolyte content of the heart revealed, furthermore, that the non-specific stimuli applied all produce a significant ionic shift: a net uptake of myocardial potassium and sometimes also of magnesium, on the one hand, and a reduction in sodium content, on the other. There was a direct relationship between the degree of protection afforded and the grade of electrolyte alterations and, consequently, it is suggested that stressor agents act through this, presumably terminal, ionic pathway in regulating the resistance of the heart muscle.