Glycogenolysis in the Anoxic Heart

¹ From the Department of Medicine, Emory University School of Medicine, Grady Memorial Hospital, Atlanta, Georgia

It has been generally accepted that cardiac anoxia caused glycogen depletion and epinephrine was implicated as a mediator in this glycogenolysis. Recently, work has shown that epinephrine and norepinephrine produce an increase in cardiac glycogen rather than glycogen depletion in the rat. Since cardiac work was not considered in previous studies, the present experiment was designed to test the effect of work on glycogenolysis of the anoxic heart in vivo and in vitro. Unfasted rats were anesthetized and observations were made on intact rats with anoxia resulting from an open chest. In vitro studies were performed on rapidly excised hearts studied in room air, in saline and in nitrogen. After 4 minutes of anoxia in the open chest 83% of the control glycogen was lost and no difference was noted whether or not the adrenal medullae were present. When the large vessels were severed, much less glycogenolysis occurred in the anoxic heart. No glycogen decrease was observed in the excised heart beating 4 minutes in room air or in nitrogen, but significant glycogenolysis was observed in the anoxic heart beating 4 minutes in saline. The anoxic heart severed from the circulation has shown no glycogenolysis whereas the anoxic heart with intact circulation showed marked glycogenolysis. It would appear from this experiment that anoxia per se was not the cause of glycogen decrease but that the amount of work performed by the anoxic heart was the critical factor in producing glycogenolysis. When a work load was placed on the excised heart beating in saline, glycogen decrease was observed. Epinephrine has been excluded as the cause of glycogenolysis in the anoxic heart since comparable cardiac glycogen changes were observed during anoxia in normal and adrenal demedullated rats.