Investigations Regarding the Etiology of Acute Exertional Rhabdomyolysis Using an Animal Model.
Abstract
The purpose of these studies was to establish whether acute exertional rhabdomyolysis could be produced in potassium- or magnesium-deficient dogs. In addition, attempts were made to induce exertional rhabdomyolysis in control dogs by repetitive exhaustive exercise of gracilis muscles. Exertional rhabdomyolysis was induced in the exercised gracilis muscle of one potassium deficient animal. No evidence of rhabdomyolysis was observed in any of the other six potassium deficient animals nor in the magnesium deficient dogs. No evidence of rhabdomyolysis was observed in the gracilis muscles of control dogs whose muscles were exhaustively exercised, allowed to rest for various time intervals, and then re-exercised. In vitro metabolic studies of potassium- and magnesium-deficient muscles revealed that optimal glycogenolysis and glycolysis occurred at concentrations of these ions far below that seen in the muscle cell water of such muscles. We concluded that a functional impairment of glycogenolysis and glycolysis is not the mechanism by which potassium and magnesium deficiencies lead to rhabdomyolysis. (Author)
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 1975
- Accession Number
- ADA014560
Entities
People
- Harold W. Carroll
- John E. Olerud
- Robert L. Eason
- William H. Pryor Jr.