Abstract
Summary
We have presented evidence that in an in vitro system, glycogenolysis and glycolysis function normally at potassium levels far below those observed in muscle cell water of severely deficient dogs. We suggest that a functional impairment of glycogenolysis or glycolysis is unlikely to be a mechanism by which potassium deficiency leads to rhabdomyolysis.
The authors wish to acknowledge the invaluable technical assistance of Mr. H. J. Burns, Jr., HM1 C. Causey, Mr. R. Jackson, and Mr. J. Hamby.
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