Comparative analysis of reparative reactions in the anterior tibialis muscles of OXYS and Wistar rats after intramuscular injections of bupivacaine was carried out for eva, luating the regeneratory potential of skeletal muscles under conditions of chronic disorders of oxidative metabolism. Lumpy degradation of lesion foci and mononuclear cell infiltration predominated on day 1; after 3 days myoblast proliferation and fusion processes were maximally pronounced; after 7 days maturing myotubules created groups of fibers with central nuclei. At the ultrastructural level, regeneration of the muscle fibers was associated with signs of activation of their nuclei and of satellite cell nuclei. Lesser (in comparison with the control) mean cross-section areas of the muscle fibers on day 14 after the start of the experiment indicated that the regeneration processes were not completed by this term. The proliferative potential of myogenic precursor cells was retained in hereditary dysfunction of mitochondria in OXYS rats.

Sixty-four male Wistar rats were subjected to repeated complete starvation with free access to water. Each starvation period lasted 6 days and was followed by a 7-day recovery period. The concentrationof cardiomyocytes (CMC) and their total number in the left ventricle (LV) were measured after alkaline dissociation of the myocardium. The volume density of muscle fibers and their absolute total mass in the LV were determined by stereological analysis. It is shown that after 6 successive starvation periods the proliferative potential of the CMC population is reduced. Key Words: starvation period; rat myocardium; cardiomyocytes, cell populationStarvation is one of the factors reducing the synthesis of structural proteins in animal tissues and organs with a parallel decrease in the mass of parenchymatous organs. The latter phenomenon has been less studied than the body mass loss. In numerous experiments on albino mice and rats it was demonstrated that after starvation is discontinued the animals grow in accordance with their body weight [12]. However, in the case of repeated starvation the compensatory growth slows down, and after several starvation periods (5-7 for rats) free access to food does not provide for the full recovery of body weight, and the animals die of unknown causes [2].It is generally accepted that the decrease in the heart mass is determined by the total decrease in the mass of the parenchymatous cells; however, the cellular mechanisms underlying this decrease Modeled fast has often been used for morphological studies of the myocardium [3][4][5][6][7]10]. The objective of this study was to investigate the dynamics of the number of the parenchymatous cells of the heart during repeated starvation periods and to fred out which processes are responsible for the compensatory growth of the mass of the myocardial muscular component during the recovery periods after starvation. MATERIALS AND METHODSThe experiments were performed on 64 male Wistar rats. The animals were assigned to 8 equal groups (n=8): 2 control and 6 experimental. The rats of the experimental groups were subjected to a 6-day total starvation with free access to water [7]. The animals were kept in individual wire bottom cages with to prevent cannibalism and co-

Hypertrophy, atrophy, and dystrophy, which reflect the balance between alterative and compensatory-adaptive processes at all levels of structural organization, predominate among structural changes in W/SSM rats with metabolic myopathy under conditions of progressive chronic disorders of cellular homeostasis. Primary universal reactions of striated muscles to damage (myofibril contractures and intracellular myocytolysis) are observed at the ultrastructural level. Increased incidence of focal changes and the time course of morphological and stereologieal parameters in a constantly functioning organ (diaphragm) indicate that working muscle fibers are most susceptible to injury.