Skeletal muscle injury after magnesium depletion in the dog

Magnesium deficiency was induced in a setting of an otherwise adequate diet in adult beagle dogs. Despite the development of severe hypomagnesemia (from 1.5 ± 0.2 to 0.5 ± 0.2 meq/liter) during the 10-wk study, Mg content of skeletal muscle fell only modestly (from 3.8 ± 0.2 to 3.1 ± 0.4, P < 0.005, at 7 wk and 3.5 ± 0.4 mM/100 g FFDS, NS, at 10 wk). The most pronounced muscle compositional changes were a loss of phosphorus (from 29.5 ± 1.8 to 22.0 ± 1.6, P < 0.001, at 7 wk and 24.8 ± 2.8 mM/100 g FFDS, P < 0.001, at 10 wk) and gains of calcium (from 0.64 ± 0.11 to 0.93 ± 0.17, P < 0.05, at 7 wk, and 0.85 ± 0.26 mM/100 g FFDS, P < 0.05, at 10 wk), sodium (from 13.2 ± 2.6 to 22.9 ± 4.7, P < 0.001 at 7 wk and 17.8 ± 2.0 meq/100 g FFDS, P < 0.005, at 10 wk), and chloride (from 5.8 ± 0.8 to 8.2 ± 1.6, P < 0.001, at 7 wk and 6.8 ± 0.6 meq/100 g FFDS, P < 0.05, at 10 wk). Cellular potassium content did not change (from 35.9 ± 1.9 to 33.0 ± 4.1, NS, at 7 wk and 36.3 ± 2.0 meq/100 g FFDS, NS, at 10 wk). Muscle cell electrical hyperpolarization developed after 10 wk of Mg depletion. Convulsive seizures developed in three animals. Frank rhabdomyolysis in three animals and focal necrosis in four animals were present on terminal biopsy, with only four animals having completely normal histology.