Structural and functional changes of the contractile proteins in experimentally-induced cardiac hypertrophy in animals, and heart failure in man

Abstract

During the first acute stage of heart over-loading after experimentally-induced aortic stenosis, the ATPase activity of isolated actomyosin and the contractility of glycerinized fibrils from the left ventricle decrease. The restoration of the initial ATPase activity level and contractility of the fibrils takes place with the development of hypertrophy, during 3 months. The second stage—relatively stable cardiac hyperfunction (6 to 8 months after coarctation of aorta in dogs)—is characterized by an increased enzymic activity of the contractile proteins and some changes in their physicochemical properties (increase of absorption in the u.v. region, decrease of K m and V max for the reaction of tryptic digestion, values of Δ n and “melting” point of myosin). At the same time, a significant activation is observed in the ATPase of the contractile proteins by strophanthin, as well as a marked myosin “anomaly” in neutral pH medium. Our results indicate the production of local changes in the HMM region of myosin. The detected phenomena suggest the possibility of the synthesis of a new myosin population (ATPase isozyme), at the stage of relatively stable cardiac hypertrophy. The investigation of the contractile proteins of biopsied left auricles from patients with mitral stenosis has demonstrated significant changes in their enzymic activity and other characteristics in accordance with the reduction in the degree of circulatory adaptability to exercise.