Effect of Epinephrine on the Oxygen Consumption of Frogs Before and After Hepatectomy.

It has been shown that epinephrine injections in physiological doses liberate lactic acid in muscle. From the work of Meyerhof it is known that an increased formation of lactic acid in muscle is followed by increased respiration. The calorigenic action of epinephrine is ascribed to the extra expenditure of energy required in the reconversion of lactic acid to glycogen. This conception raises the following 2 questions: 1. In what tissues is the reconversion of lactic acid taking place? 2. What is the efficiency of the reconversion process? The present experiments deal mainly with the first question.

Frogs were used with the central nervous system destroyed with the exception of the medulla oblongata. Such animals are able to breathe spontaneously but otherwise they are completely immobilized. Oxygen consumption (at 15° C.) was determined by connecting glass vessels, in which the frogs were placed, with Warburg manometers, the CO₂ being absorbed by KOH. Table I shows that the average oxygen consumption during 2 basal hourly periods is of practically the same magnitude. After the second basal hour the frogs were removed from their containers and injected with salt solution in order to test the effect of an injection. A slight increase in O₂ consumption was noted. A subsequent injection of 0.05 to 0.1 mg. of epinephrine into a lymph sack was followed by a marked rise in O₂ consumption, lasting for 2 hours. This result dispels the notion held by some investigators, that the increased O₂ consumption after epinephrine injection is of central origin and is due to the hyperactivity of the animal.

The immobilized frogs were hepatectomized. A calorigenic effect of epinephrine, nearly as marked as in frogs with intact liver, was obtained on the first day after hepatectomy.