CHANGES IN THE ULTRASTRUCTURE OF THE LEFT VENTRICULAR MYOCARDIUM DURING THE ONTOGENESIS OF WISTAR RATS

Abstract

The conducted studies demonstrate significant changes in the ultrastructure of cardiomyocytes of the myocardium of the left ventricle during the late embryonic and early postnatal development of Wistar rats. A series of images of the ultrastructure of contractile myocytes of rats of different chronological ages made it possible to obtain morphological information about the gradual complication of the spatial organization and saturation of the sarcoplasm with myofibrils and mitochondria – a complex of organelles responsible for the contractile function of the myocardium. The role of positional information in the interaction of structural elements of the complex (myofibrils + mitochondria) has been investigated. Morphological manifestations of the development of physiological apoptosis of cardiomyocytes in the process of pre- and postnatal development of the myocardium of Wistar rats were identified and investigated. In the process of postnatal maturation of the CMC, there is a continuous increase in the relative volumes of MF and MH. In 45 days, the relative volume of MF increases from 33% to 40%, and the relative volume of MH increases from 21% to 40%. The parenchyma of the myocardium of newborn rats is formed by three unequal populations of CMCs. The first population is mononuclear dehydrated myocytes that form a reserve of CMCs and are in a state of functional rest. The second population is mononuclear optically bright myocytes, which have contractile and proliferative functions and are subject to physiological hypertrophy. The third population is binucleated cardiomyocytes (2a-CMC), the number of which increases within 15 days after the birth of rats. In the process of early postnatal development of rats, in the parenchyma of the myocardium between the three interacting populations of CMCs, there is the following sequence of transformations: 1a t-CMCs → 1a c-CMCs → 2a-CMCs. The appearance of deformed CMC nuclei in the myocardial parenchyma is caused by short-term “nucleus + organelle” contacts and pulsed mechanical pressures on the nuclei from the side of myofibrils and mitochondria in the process of continuously repeating cycles (contraction ↔ relaxation) of CMC.