Biomedical subjects
Publications and source records attributed to M G Klinnikova.
Single total hyperthermia changed the absolute number of cardiomyocytes in experimental animals. The total number of cardiomyocytes decreased by 20% (without signs of their necrosis) on day 3 of post-heating restitution and then returned to the control. This was probably related to cytokinesis (without karyokinesis) of binucleated cells, whose content considerably decreased during recovery.
hyperthermia caused hemodynamic disorders in the liver and degenerative and necrobiotic changes in hepatocytes of CBA mice. Total hepatocyte count decreased during restitution, this decrease being most pronounced 30 min after exposure. The number of binucleated cells also markedly decreased. The absence of necrotic changes in hepatocytes during the entire restitution period indicated their apoptotic death and elimination by macrophagal resorption. Under these conditions liver regeneration at the cellular level occured mainly via division of binucleated hepatocytes. On the other hand, proliferation of oval cells in the portal zones and their differentiation into hepatocytes were observed at certain stages of reparative regeneration of the liver.
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The reorganization of Wistar rat myocardium at 3 and 7 days after a single total overheating at a temperature of 43 degrees C was studied using stereologic and qualitative morphological tissue analysis. Most pronounced morphofunctional changes in myocardium were shown to develop 3 days after the exposure such as hemodynamic disorders, lymphostasis, interstitial edema, contracture lesions of cardiomyocytes. The spatial myocardial reorganization was not considerable. At 7 day after exposure, a significant decrease of the heart weight as a result of atrophic changes in cardiomyocytes was recorded. In the same period the most pronounced spatial reorganization of myocardial parenchyma and stroma was noted. The significant decrease of volume density of capillaries was accompanied by some increase of the volume density of cardiomyocytes resulting in a significant decrease of volume ratio of capillaries to cardiomyocytes. Thus, during postheating restitution the atrophy of myocardium developed characterized by an unbalanced decrease of volume densities of capillaries and cardiomyocytes.
A comparative morphologic study of Wistar rat myocardium under contrast temperature influences (extreme and moderate general cooling and general overheating) was carried out. It is shown that different regimens of general cooling and general overheating cause dramatic structural changes in the myocardium both at the tissue and subcellular levels. Tissue changes manifested as hemodynamic disorders, contracture and lytic injuries to cardiomyocytes resultant in necrobiosis and atrophy of some cardiomyocytes. These changes were more pronounced under acute influences. Tissue spatial myocardium reorganization had a stereotype pattern. Quantitative changes of main parenchymatous and stromal structure did not differ significantly under various temperature regimens. At subcellular level more pronounced quantitative and qualitative changes of organelles were revealed under general cooling irrespectively of the duration of the experimental exposure.