Rates of actin polymerization and of contractility of myocardial glycerinated fibers (the myofibrillar contractile system) were found to be decreased in patients with myocardium infarction and in experimental heart ischemia. The phenomena were noted within the earliest period under study (I hr after development of ischemia). Causes of the decrease in the rates of actin polymerization and of the myofibrillar contractility did not involve hypoxia and acidosis. They were observed in non-ischemic and non-infarcted zones of left ventricles and in non-impaired right ventricles. The data obtained suggest that alterations in physico-chemical properties of actin (the main protein of thin myofilament) leading the decrease in the contractile functions, were responsible for acute failure of heart muscle in ischemia and infarction.
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