Mechanism of physiologic versus pathologic ventricular hypertrophy process: Enhanced or depressed myosin ATPase activity and contractility governed by type, degree and duration of inciting stress

Wikman‐Coffelt, Joan; Laks, Michael M.; Riemenschneider, Th.; Mason, Dean T.

doi:10.1007/978-3-662-41468-2_21

Experimental Cardiac Hypertrophy and Heart Failure 1980

DOI: 10.1007/978-3-662-41468-2_21

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Mechanism of physiologic versus pathologic ventricular hypertrophy process: Enhanced or depressed myosin ATPase activity and contractility governed by type, degree and duration of inciting stress

Joan Wikman‐Coffelt¹,

Michael M. Laks²,

Th. Riemenschneider³

et al.

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1986

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Cited by 4 publications

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Thin myofilament proteins in norm and heart failure I. Polymerizability of myocardial Straub actin in acute and chronic heart failure

Карсанов¹,

Pirtskhalaishvili²,

Semerikova³

et al. 1986

Basic Res Cardiol

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The reduced and intrinsic viscosities of myocardial Straub F-actin from the left ventricle of a practically healthy man were equal to 3.05 +/- 0.2 and 2.4 +/- 0.32 and from the right ventricle were 2.37 +/- 0.2 and 2.1 +/- 0.3 dl/g, respectively (the difference between ventricles was not significant). The average length of filaments measured by flow birefringence technique was equal to 1.3 +/- 0.04 micron, the number-average length (Ln), determined by the electron microscopy was 1.4 micron, the weight-average length (Lw), was 2 microns and the maximal one was 5.5 microns. The histograms showed that the most characteristic length was that of 0.8-1.2 micron. According to the flow birefringence data canine myocardial F-actin had a length similar to that of myocardial F-actin from a practically healthy man, though its reduced and intrinsic viscosities were higher. In acute and especially chronic congestive heart failure the actin polymerizability was sharply reduced. In consequence, in acute heart failure the number-average length of F-actin filaments was decreased by 43% and in congestive heart failure by 65.7%. The characteristic length in acute heart failure shifts to the range of 0.2-0.6 micron, while in congestive heart failure the range is 0.2-0.4 micron. This fact can possibly explain why during preparation of actin from the pathologically changed myocardium according to the methods including purification by the cycles of polymerization-sedimentation-depolymerization, the pathologically changed actin is discarded and the normal actin remains. A definite parallel was observed between the reduction of actin polymerizability and the ability of myocardial glycerinated fiber bundles (MBGF) to generate force. We conclude that the changes of actin properties in heart failure may cause a decrease in contractibility of the myocardial contractile protein system.

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Thin myofilament proteins in norm and heart failure I. Polymerizability of myocardial Straub actin in acute and chronic heart failure

Карсанов¹,

Pirtskhalaishvili²,

Semerikova³

et al. 1986

Basic Res Cardiol

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Subcellular bases of cardiac disturbance in experimental informational neurosis

Khananashvili

Карсанов

1987

International Journal of Psychophysiology

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The cardiac hypertrophy process. Analyses of factors determining pathological vs. physiological development.

Wikman‐Coffelt¹,

Parmley²,

Mason³

1979

Circulation Research

265

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COMPLICATED and even contradictory concepts concerning the biochemical and physiological aspects of cardiac hypertrophy are less enigmatic if we first discern whether the type of hypertrophy analyzed is physiological or pathological; i.e., whether factors secondary to the process of hypertrophy have induced the heart to augment or depress its mechanical function. In this review physiological hypertrophy is defined as hypertrophy accompanied by a normal or augmented contractile state in which the maximum rate at which myosin hydrolyzes ATP and the maximum velocity of muscle shortening are either normal or elevated. Pathological hypertrophy, on the other hand, is associated with depressed contractility without necessarily concordant heart failure, in which case the rate of myosin ATPase activity and the velocity of muscle shortening are decreased. Both types of hypertrophy may be considered compensatory in that the heart biochemically and physiologically adjusts to cellular alterations that occur according to the severity of the workload. Thus, our definition is not the same as that provided by Meerson (1976), since he did not distinguish between the two types of hypertrophy described here.To understand better the evolution of the cardiac hypertrophy process into physiological or pathological hypertrophy, this review is concerned with the immediate inciting stimuli of cardiac hypertrophy, the mechanism of its development, the various stages in its development, and its regional localization. We also are concerned with the dependency of

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Mechanism of physiologic versus pathologic ventricular hypertrophy process: Enhanced or depressed myosin ATPase activity and contractility governed by type, degree and duration of inciting stress

Cited by 4 publications

References 14 publications

Thin myofilament proteins in norm and heart failure I. Polymerizability of myocardial Straub actin in acute and chronic heart failure

Thin myofilament proteins in norm and heart failure I. Polymerizability of myocardial Straub actin in acute and chronic heart failure

Subcellular bases of cardiac disturbance in experimental informational neurosis

The cardiac hypertrophy process. Analyses of factors determining pathological vs. physiological development.

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