Compensatory and adaptive reactions of the ultrastructures of the myocardium and its microcirculatory bed in conditions of adaptation to a cold environment

Functional hemodynamic restructuring under the influence of low temperature exposure has been given sufficient attention, however, the structural support of the intensively functioning myocardium in the conditions of its adaptation to cold has not yet been fully studied. The purpose of the study: to identify the ultrastructural foundations of myocardial adaptation to cold, to determine the dynamics of compensatory restructuring at the tissue and cellular levels. The sixteen-week experiment was conducted on outbred white rats (260 males and 190 females) during the period of progressive growth, starting at four weeks of age. The experimental group of animals was kept in a room, in which the temperature was constantly maintained at 4±1 °C. The control group of animals was kept in a room with a temperature of 20±10 °C. Animals were removed from the experiment after preliminary anesthesia after 1, 3, 5, 7, 14, 28, 42, 84, 112 days of cold adaptation, taking into account data on the periodization of biological processes. The following research methods were used: macromorphometric study of the heart; histological study of paraffin sections stained with hematoxylin-eosin, Heidenhain's Iron Hematoxylin, according to Mallory, Crossman, Van Gieson, Gomori's silver impregnation method; ultrastructural and micromorphometric study of semi-thin sections 1 μm thick, stained with 0.1 % toluidine blue solution; stereological study of electron diffraction patterns. Statistical processing of the obtained results was carried out using the SPSS, STATISTICA v. 10.0 statistical software package. It was found that in the process of myocardial adaptation to cold the stages of urgent and long-term adaptation are observed. Urgent adaptation should be considered as a pronounced stress reaction, which is characterized by violation of hemodynamics and the intense functioning of intracellular organelles of cardiomyocytes and, as a result, their destruction and autophagy. Stressed functioning of myocardial structures and energy starvation leads to changes in the transcriptional program, activating the expression of genes associated with the synthesis of nucleic acids and proteins and the expression of genes associated with the activation of fibroblasts, which plays a decisive role in the development of cardiac hypertrophy. Myocardial hypertrophy with active capillary neoplasm reaches its maximum degree in the fourth week of the experiment. After the eighth week of adaptation, the degree of myocardial hypertrophy gradually decreases, the morphological picture of the heart muscle normalizes. A characteristic feature of cardiomyocytes during long-term adaptation is the accumulation of mitochondria, mainly small and medium-sized, with parallel, densely packed cristae and their saturation with glycogen granules. Myocardial capillaries often take a tortuous course, some of them are closed and reduced. Thus, in the process of long-term adaptation, a “structural trace” is formed in the heart, which is manifested by myocardial hypertrophy, mitochondrial hyperplasia, glycogen accumulation in cardiomyocytes and capillary neoplasms. These compensatory mechanisms create a functional, energy and hemodynamic reserve in the heart muscle.