THE TACHYCARDIA, TIME FACTOR, SURVIVAL PERIOD AND SEAT OF ACTION OF THYROXINE IN THE PERFUSED HEARTS OF THYROXINIZED RABBITS
- 1 September 1931
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Legacy Content
- Vol. 98 (2), 338-343
- https://doi.org/10.1152/ajplegacy.1931.98.2.338
Abstract
Perfused hearts of 23 acutely thyroxinized rabbits beat much faster than hearts of non-thyroxinized rabbits, as previously shown by others. In 17 hearts studied there was a latent period of about 2 days following intravenous injection of thyroxine before this acceleration was noted. As shown by serial perfusion experiments, the heart continues to beat very rapidly for about 12 days and then returns to the normal rate in about 17 days after the injection. Within certain limits, dosage seems to have little effect on the degree of tachycardia; this probably means that the smallest dose used was maximal. The survival period of 12 hearts, sufficiently thyroxinized to make them strongly hyperthyroid, was not significantly different from the survival period of non-thyroxinized hearts. The hearts of thyroxinized animals were more subject to attacks of arrhythmia and seemed to beat more vigorously than normal. After excision of the sino-auric-ular node of the perfused heart of 6 acutely thyroxinized rabbits, the heart rate was still greatly increased. When auriculoventricular dissociation was produced by crushing the bundle of His the ventricles usually beat at an accelerated rate. These results mean that the auricles and ventricles independently beat faster than normally. Thyroxine seems to exert its effect, therefore, upon all parts of the heart. This study does not indicate whether the action of thyroxine is upon the muscle fibers or upon the nerve endings in the myocardium, but studies now being made by Cecile Markowitz give reason to believe that it is directly upon the muscle cells.This publication has 1 reference indexed in Scilit:
- OSMOTIC PRESSURE, BOUND WATER AND EDEMA IN PERFUSED HEARTSAmerican Journal of Physiology-Legacy Content, 1931