Augmented right ventricular function in systemic hypertension-induced hypertrophy

Pool, Peter E.; Piggott, William J.; Seagren, Shirley C.; Skelton, C. Lynn

doi:10.1093/cvr/10.1.124

Cited by 25 publications

(7 citation statements)

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“…In agreement with these observations are the findings in the hemodynamically stressed left ventricle and nonstressed right ventricle in experimental systemic hypertension (Pool et al, 1976). In other studies of the nonstressed right ventricle in hearts with a hypertrophied pressureoverloaded left ventricle, the inotropic state of right ventricular papillary muscle was elevated (Pool et al, 1976). Moreover, investigations recently carried out in our laboratories on pulmonary artery-or aortic-banded dogs demonstrated similar temporal alterations between the two ventricles.…”

Section: Progression Of Myocardial Hypertrophysupporting

confidence: 80%

“…Thus, it appears that sustained, moderate ventricular outflow obstruction may lead to pathological hypertrophy. In agreement with these observations are the findings in the hemodynamically stressed left ventricle and nonstressed right ventricle in experimental systemic hypertension (Pool et al, 1976). In other studies of the nonstressed right ventricle in hearts with a hypertrophied pressureoverloaded left ventricle, the inotropic state of right ventricular papillary muscle was elevated (Pool et al, 1976).…”

Section: Progression Of Myocardial Hypertrophysupporting

confidence: 73%

“…Thus, under this condition, myosin ATPase activity is temporarily increased (Wikman-Coffelt, et al, 1975b, 1975c, whereas contractile function remains normal (Meerson, 1969) or even is elevated (Meerson, 1969;Stewart et al, 1978). An increase in contractile state of the nonstressed ventricle also was associated with hypertrophy of this chamber in experimentally induced systemic hypertension (Pool et al, 1976). It is possible that this type of physiological hypertrophy may gradually return to normal metabolic and mechanical activity.…”

Section: Progression Of Myocardial Hypertrophymentioning

confidence: 99%

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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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Section: Progression Of Myocardial Hypertrophysupporting

confidence: 80%

Section: Progression Of Myocardial Hypertrophysupporting

confidence: 73%

Section: Progression Of Myocardial Hypertrophymentioning

confidence: 99%

See 1 more Smart Citation

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

Wikman‐Coffelt¹,

Parmley²,

Mason³

1979

Circulation Research

265

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“…We did not measure right ventricular or pulmonary arterial pressure. However, several investigators have reported an association between right and left ventricular hypertrophy (11,27,28), with some suggesting a hypertensive relation between the systemic and pulmonary vascular beds (2) and others stating the right ventricular hypertrophy in left ventricular pressure overload was independent of right ventricular hypertension (16).…”

Section: Discussionmentioning

confidence: 99%

Change in cardiac myocyte size distribution in aortic-constricted neonatal rats

1989

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Regional changes in cardiac myocyte size and population distribution were examined in Sprague Dawley rats receiving an abdominal aortic constriction at five days of age. At specific time intervals post-constriction, hearts were recovered from constricted animals and weight-matched controls and isolated myocytes were obtained from right and left ventricles using retrograde coronary perfusion with collagenase. Cell volume and cardiac myocyte population distribution curves were determined using a Coulter Channelyzer system. Cell length was measured directly using a Bioquant Image Analysis system. Myocyte cross-sectional area was calculated from cell volume/length. By three months of age, heart weight and heart weight-body weight ratio in constricted animals had increased by approximately 115% (p less than 0.001) in females and 85% (p less than 0.001) in males compared to controls. Between 15 and 90 days of age, the growth response, as indicated by increased cell volume, was approximately 4x greater in constricted females and 2.5x greater in constricted males compared to corresponding controls. This increase was manifested by a shift in the mean size of the myocyte population to the right and a substantial widening of the distribution. Most of the enlargement was due to increased cross-sectional area, with only a moderate contribution from increased cell length. Significant increases in size were seen in both left and right ventricles. By three months of age, a significant interaction was apparent between aortic constriction and sex. The capacity for hypertrophy was greater in the smaller myocytes in female rats of similar age compared to males. The final degree of hypertrophy was similar for male and female rats, possibly indicating a critical upper limit in cell size for cardiac myocytes.

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“…These echocardiographic findings are in keeping with previous reports in experimental animals about the pathophysiology of inter-ventricular interaction. Left ventricular pressure overload induced by proximal aorta banding in experimental animals was found to be associated with increased biochemical and haemodynamic function of the 'nonstressed' ventricle as well as with development of biventricular hypertrophy [30]. Furthermore, banding of the dog pulmonary artery, in addition to causing right ventricular wall thickening, resulted in increased left ventricular mass and stiffness [31].…”

Section: Hypertensive Right Ventricular Hypertrophymentioning

confidence: 99%