MECHANISM OF THE EFFECT OF HYPERTHYROIDISM ON CARDIAC GLYCOGEN

Abstract

Methods were de-veloped for accurate and consistent detn. of heart rate, O2 consumption, and cardiac glycogen in the white rat. A technique was also devised for the removal of large amts. of blood from the rats tail. Standard predictable levels of heart rate and basal metabolic rate were established in 110 rats. After approx. 2 weeks exptl. manipulation, cardiac glycogen contents were detd. and compared, in relation to the changes produced in heart rate and metabolic rate, with normal controls and with each other. Moderate hyperthyroidism was found to deplete heart glycogen to an extent directly related to the increase in heart rate but not closely related to the metabolic stimulation. Atropine and chilling (by depilation) decreased heart glycogen, in relation to the tachycardia produced, to a degree similar to that obtained in hyperthyroidism. Caffeine caused a smaller loss of heart glycogen, with reference to the stimulation of heart rate, than would have been predicted from the effects of thyroid, atropine, and chilling. This might have resulted from the increased blood pressure and the coronary dilatation characteristic of caffeine medication. Primary anemia produced a decrease in heart glycogen roughly correlated with the decline in Hb content of the blood. Co poly-cythemia seemed, to a slight extent, to protect the hyper-thyroid heart from loss of its glycogen stores. The decrease in heart glycogen of 19 hyperthyroid rats was participated in by both the left and right ventricles. Loss by the left ventricle was greater by an avg. of 37%, but the variability of results, due to technical difficulties, renders this difference not statistically as significant as might be desired. It is concluded that the decrease in heart glycogen by hyperthyroidism is not due to any specific toxic influence of the thyroid hormone. The suggestion is tentatively offered that the glycogenolytic action is exerted through a relative ischemia caused directly and indirectly by the increased cardiac activity.