Mechanism for the Abnormal Energetics of Pressure-Induced Hypertrophy of Cat Myocardium

Cooper, George; Satava, Richard M.; Harrison, Carlos E.; Coleman, Henry Neal

doi:10.1161/01.res.33.2.213

Cited by 107 publications

(65 citation statements)

References 41 publications

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“…Right ventricular hypertrophy was induced by partially occluding the pulmonary artery with a 3.5-mm internal diameter band. Again, full details ofthis procedure have been published before (14). Cats weighing 1.9-4.7 kg were prepared, and a thoracotomy was performed.…”

Section: Methodsmentioning

confidence: 99%

Hemodynamic versus adrenergic control of cat right ventricular hypertrophy.

Th¹,

Kent²,

Uboh³

et al. 1985

J. Clin. Invest.

137

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The purpose of this study was to determine whether cardiac hypertrophy in response to hemodynamic overloading is a primary result of the increased load or is instead a secondary result of such other factors as concurrent sympathetic activation. To make this distinction, four experiments were done; the major experimental result, cardiac hypertrophy, was assessed in terms of ventricular mass and cardiocyte cross-sectional area. In the first experiment, the cat right ventricle was loaded differentially by pressure overloading the ventricle, while unloading a constituent papillary muscle; this model was used to ask whether any endogenous or exogenous substance caused uniform hypertrophy, or whether locally appropriate load responses caused ventricular hypertrophy with papillary muscle atrophy. The latter result obtained, both when each aspect of differential loading was simultaneous and when a previously hypertrophied papillary muscle was unloaded in a pressure overloaded right ventricle. In the second experiment, epicardial denervation and then pressure overloading was used to assess the role of local neurogenic catecholamines in the genesis of hypertrophy. The degree of hypertrophy caused by these procedures was the same as that caused by pressure overloading alone. In the third and fourth experiments, fi-adrenoceptor or a-adrenoceptor blockade was produced before and maintained during pressure overloading. The hypertrophic response did not differ in either case from that caused by pressure overloading without adrenoceptor blockade. These experiments demonstrate the following: first, cardiac hypertrophy is a local response to increased load, so that any factor serving as a mediator of this response must be either locally generated or selectively active only in those cardiocytes in which stress and/or strain are increased; second, catecholamines are not that mediator, in that adrenergic activation is neither necessary for nor importantly modifies the cardiac hypertrophic response to an increased hemodynamic load.

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Section: Methodsmentioning

confidence: 99%

Hemodynamic versus adrenergic control of cat right ventricular hypertrophy.

Th¹,

Kent²,

Uboh³

et al. 1985

J. Clin. Invest.

137

View full text Add to dashboard Cite

show abstract

“…In previous studies in which depressed contractile state has been observed, the majority of experiments were performed within 60 days of banding (5,6,8,9). Furthermore, the data from muscles examined after different periods of constriction were generally grouped together.…”

Section: Contractile State Of Hypertrophied Myocardium 1269mentioning

confidence: 99%

“…Furthermore, if slight differences were observed, it would be difficult to conclude that such differences represented alterations in contractile state. The papillary muscles of the banded animals were also slightly larger and therefore more subject to hypoxia and impaired function at higher frequencies of contraction (16 (5,6,8).…”

Section: Contractile State Of Hypertrophied Myocardium 1269mentioning

confidence: 99%

Normal Contractile State of Hypertrophied Myocardium after Pulmonary Artery Constriction in the Cat

Williams¹,

Potter²

1974

J. Clin. Invest.

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A B S T R A C T The contractile function of right ventricular papillary muscles from normal cats and cats in which the pulmonary artery had been constricted for 6 or 24 wk was examined. Acute pulmonary artery constriction reduced cross-sectional area by an average of 70%, resulting in a 30% mortality from congestive heart failure, all such deaths occurring within the first 3 wk after banding. The increase in right ventricular mass in animals surviving for 6 or 24 wk was similar, averaging 70%. No banded animals had evidence of congestive heart failure at the time of sacrifice, and cardiac output and right atrial pressures were similar to those in control animals.6 wk after banding, the active length-tension curve, maximal rate of rise of isometric force, force-velocity relations, and isometric force with paired stimulation and norepinephrine were all significantly depressed when compared to their respective values in control animals. In contrast, none of these variables was significantly different from control values in animals banded for 24 wk. These observations indicate that depressed contractile state is not a fundamental characteristic of pressureinduced hypertrophied myocardium and reemphasize the important temporal relationship between contractile state and the imposition of sudden sustained loads.

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“…Thus it has been shown that the right ventricle is particularly sensitive to pressure overload, with decreases of contractility found even before clinical failure. 7 The abnormalities are still reversible until the development of overt failure. Once failure has ensued, it is no longer reversible.8 In contrast, the left ventricle seems to tolerate both pressure and volume overload for a considerable time before abnormalities of contraction can be detected.9…”

mentioning

confidence: 99%

“…16 Alternatively, this finding may show an inhibition of calcium uptake by, or release from, the sarcoplasmic reticulum in patients with heart failure. 7 (c) The production of cyclic AMP by hypertrophied and failing cardiocytes has also received a great deal of attention. The contractile response of failing myocardium to fi adrenergic stimulation by isoprenaline is subnormal."…”

mentioning

confidence: 99%

Central haemodynamic expressions of heart failure

Burkart¹

1994

Heart

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Mechanism for the Abnormal Energetics of Pressure-Induced Hypertrophy of Cat Myocardium

Cited by 107 publications

References 41 publications

Hemodynamic versus adrenergic control of cat right ventricular hypertrophy.

Hemodynamic versus adrenergic control of cat right ventricular hypertrophy.

Normal Contractile State of Hypertrophied Myocardium after Pulmonary Artery Constriction in the Cat

Central haemodynamic expressions of heart failure

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