Abstract
The reduced functional load during starvation or protein deficiency leads to reduced protein synthesis in heart muscle [11-13, 15]. Inhibition of protein metabolism associated with interruption of the supply of structural material with the food causes delay in the renewal of contractile proteins, and the unsynchronized changes in the ultrastructural organization of cardiomyocytes are connected with this [3, 4]. The principal structural manifestation of inhibition of protein synthesis when the functional load is reduced is atrophy of the myocardium [2, 6, 9]. Quantitative morphological investigations of the myocardium during starvation have revealed considerable changes in the architectonics of the cardiomyocytes during their atrophy [3, 7]. However, the character and direction of relations between the parenchyma and connective tissue in heart muscle during starvation have not been adequately studied.
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