[The dynamics of thyrotoxic heart development in experimental thyrotoxicosis]

Thyreoidin intoxication was modelled in 12 rabbits, 39 rabbits served as controls. ON THE 3RD, 7TH AND 14TH DAY OF THE EXPERIMENT PHYSIOLOGICAL AND BIOCHEMICAL INVESTIGATIONS WERE CARRIED OUT IN ORDER TO DETERMINE THE FUNCTION OF THE LEFT VENTRICLE OF THE HEART AND CONTENTS OF ADRENALIN AND NORADRENALIN IN THE MYOCARDIUM. At the same periods an electron microscopy investigation of the contractile myocardium of the left ventricle of the heart with subsequent quanitative analysis of electronograms were carried out. It was shown that clear-cut changes in the ultrastructure of the contractile myocardium and in the heart function, accompanied with accumulation of sympathetic amines in the cardiac muscle, take place already at the early periods of the experiment. The changes in the muscle cell ultrastructure were caused by a hyperfunction of the retained organells, mitochondria in particular, due to the weakening of conjugated respiration and phosphorilation processes, as well as to the exclusion from functioning of a part of mitochondria and to an increase in the loading on the myocardium. As a result, energy deficit of the cardiac muscle originated and continued to increase. Because of inclusion of the compensatory-adaptative mechanisms, which reached their maximum by the 14th day of the experiment, the processes of plastics and energy formation at the expense of hyperplasia and hypertrophy of mitochondria, were drastically intensified, which allowed the heart to function under conditions of the increasing thyreoidin intoxication.