The Influence of Epinephrin upon the Exchange of Sugar between Blood and Muscle1

In a previous communication (1) the work of Bollman, Mann and Magath (2) and of others was confirmed and extended to show that neither epinephrin, ether anesthesia nor asphyxia has any effect upon the falling blood sugar level of abdominally eviscerated dogs. It was concluded that muscle glycogen is not an available source of blood sugar in the absence of the liver and that this organ, in the absence of food, is therefore the sole source of supply for the glucose in the blood. These results indicated that the hyperglycemia which follows the administration of e&nephrin to normal animals is due to an accelerated release of blood sugar from the liver. In a recent review, Cori (3) has marshalled evidence from which he concludes that epinephrin hyperglycemia is chiefly due to a decreased utilization of sugar by the muscles. This conclusion is based on three main theses : I. The amount of glucose which had to be supplied to normal rats in order to produce a hyperglycemia of similar magnitude and duration as that caused by a certain dose of epinephrin, was such that it could not possibly be derived from preformed liver glycogen in the latter case. II. Simultaneous determinations of arterial and venous blood sugar levels in men and in rabbits have shown that for the same degree of hyperglycemia, the arterio-venous blood sugar difference is greater when the hyperglycemia is caused by sugar administration than when it is due to epinephrin injection. III. Colwell and Bright (4) have reported that when epinephrin and glucose are continuously injected into amytalized cats, the non-protein respiratory quotient (instead of rising progressively as under identical conditions without epinephrin) drops to the fat level within 3 to 5 hours, and remains there as long as the epinephrin administration persists. These