Carbohydrate Metabolism in Degenerated Striated Muscle.

Abstract

Twenty-three rabbits used in these experiments were put under light ether anesthesia, and the gastrocnemius muscle injured either by freezing with carbon dioxide snow or by multiple light blows. After 24 to 72 hours the animals were given amytal intraperitoneally and the gastrocnemii removed after being frozen solidly with carbon dioxide snow and ethyl chloride. 1 The muscles were analyzed quantitatively for glycogen, 2 lactic acid, 3 , 4 and organic and inorganic phosphorus. 5

The average glycogen value in normal rabbit gastrocnemii was 603 mg. per 100 gm. of muscle. This dropped to 258 mg. in those muscles injured by previous freezing, and to 103 mg. in the contused muscles. From microscopic studies of the lesions it was evident that degenerative changes were more profound in the contused than in the frozen muscles. With this decrease of glycogen there was a concomitant increase of lactic acid from a control average of 19 mg. per 100 gm. of muscle, to 53 mg. in the frozen muscles and 66 mg. in contused muscles. Phosphocreatine decreased markedly from an average control value of 66.3 mg. per 100 gm. to 7 mg. in the contused muscles. Contrary, however, to expectations the inorganic phosphorus likewise decreased slightly, from 44.5 to 36.1 mg. per 100 gm.

Microscopically there was extensive molecular degeneration of the muscles, with consequent interference with the capillary blood circulation, although the larger vessels had free circulation.

The results given suggest damage to the glycogenic function or to the glycogen storing capacity of the muscles. The still-active glycogenase depleted the muscle glycogen store, with the subsequent formation of lactic acid. While some of the acid may have diffused out into the surrounding tissues or larger vessels, enough remained to show the character of the change.