Pathogenesis of "Electrolyte-Steroid-Cardiopathy"

Abstract

The production of acute necrotic lesions of the myocardium and concomitant changes in myocardial and skeletal muscle potassium concentrations were investigated in rats. Lesions were induced by the administration of 2α inethyl-9α-chlorocortisol plus oral Na ₂ SO ₄ (which caused a profuse catharsis), steroid plus an irritant cathartic (croton oil), steroid plus low-potassium diet, and low-potassium diet alone. Lesions in the various groups were grossly and microscopically indistinguishable. Their incidence and severity were well correlated with the degree of myocardial potassium depletion below a threshold value of approximately 72 mEq./Kg. wet weight. Skeletal muscle potassium was decreased roughly parallel to that of the myocardium, but some what more variably. Other treatments, including steroid or oral Na ₂ SO ₄ alone and steroid plus subcutaneous Na ₂ SO ₄ which failed to produce comparable reductions in myocardial potassium, failed to induce morphological lesions. Any specific interaction between steroid and electrolyte in the production of the myocardial lesions appears to be ruled out by the ineffectiveness of Na ₂ SO ₄ administered sub cutaneously. It is concluded that the "electro lyte-steroid-cardiopathy" results from a simple intracellular potassium deficiency and its sequelae, and that the roles of the steroid-cathartic electrolyte, and other agents and procedures are to induce potassium depletion by various mechanisms.