We investigated the possible role of potassium deficiency, a recognized cause of myopathy, in the pathogenesis of experimental acute alcoholic myopathy (EAM) in the rat. Alcohol-treated animals receiving the same dietary potassium as controls developed mild hypokalemia; however, muscle potassium was preserved or elevated even in the presence of scattered muscle fiber necrosis. Increasing dietary potassium raised serum potassium but did not prevent EAM. These data indicate that hypokalemia in EAM is due to potassium redistribution between intra- and extracellular compartments rather than potassium deficiency, and confirm clinical observations that alcohol-induced muscle injury occurs independently of potassium deficiency.
ASJC Scopus subject areas
- Clinical Neurology