Abstract
Compensatory hyperfunction of the heart in vitium cordis, hypertension and other diseases of the circulatory system connected with the cardiac overstrain of long duration represents the main factor in preservation of normal hemodynamic indices and clinical compensation. The rate of protein synthesis in the myocardium was studied under conditions of compensatory cardiac hyperfunction provoked by experimentally induced vitium cordis. As established, rapid development of hypertrophy during the first emergency stage of compensatory hyperfunction is accompanied by an intensified rate of protein synthesis (it about doubles). In the second stage of relatively stable hyperfunction the rate of protein synthesis is normal, while at the third stage — characterized by cardiosclerosis and progressive exhaustion —it is reduced 2–2.5 times. This depression of the normal renovation process of the protein myocardial structures may bring about a change in the contractile proteins of the heart, thus playing an important role in the development of cardiosclerosis and cardiac insufficiency.
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