EFFECTS OF HYPERTROPHY AND HEART-FAILURE ON [NA+](I) IN PRESSURE-OVERLOADED GUINEA-PIG HEART

被引：26

作者：

JELICKS, JA

SIRI, FM

机构：

[1] Departments of Physiology and Biophysics, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY

[2] Medicine, Albert Einstein College of Medicine, Yeshiva University, Bronx, NY

来源：

AMERICAN JOURNAL OF HYPERTENSION | 1995年 / 8卷 / 09期

关键词：

MYOCARDIAL HYPERTROPHY; HEART FAILURE; SODIUM; NA-23 NUCLEAR MAGNETIC RESONANCE; PERFUSION PRESSURE;

D O I：

10.1016/0895-7061(95)00219-F

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

Intracellular free sodium levels ([Na+](i)) were assessed with Na-23 nuclear magnetic resonance (NMR) spectroscopy in isolated, Langendorff-perfused normal, compensated hypertrophied, and hypertrophied failing guinea pig hearts under several conditions. Baseline [Na+](i) measured with a shift reagent was significantly greater than normal in the compensated hypertrophied hearts (12.8 +/- 1.2 mmol/L v 6.4 +/- 0.7 mmol/L, means +/- SEM, P < .01), but not in the hypertrophied failing hearts (8.7 +/- 1.9 mmol/L, P = N.S.). Moreover, the highest levels of [Na+](i) were seen just 3 to 4 weeks after aortic constriction. [Na+](i) was inversely related to both time after aortic constriction (R = -0.71, P < .03) and to the degree of left ventricular hypertrophy (R = -0.79, P < .01), suggesting that the hypertrophied failing heart is capable of maintaining relatively normal [Na+](i). In addition, triple quantum filtered NMR measurements were made to assess changes in [Na+](i) subsequent to altered perfusion or loading conditions. In hypertrophied failing hearts, but not normal hearts, low coronary perfusion pressure (60 cm H2O) was associated with relatively higher [Na+](i) (ANOVA, P < .05), suggesting greater sensitivity of hypertrophied failing hearts to hypoperfusion. On the other hand, when all hearts were perfused at 90 cm H2O and intraventricular balloon volume was increased from 100 mu L to 300 mu L, [Na+](i) increased significantly only in the normal guinea pig hearts (12.3 +/- 1.8%, P < .01). These findings suggest complex changes in the expression or modulation of proteins involved in Na+ regulation. Interpretation regarding the physiological significance of these changes depends on the specific mechanism(s) proposed. Previous work in this and other models of hypertrophy suggest that changes in the number or activity of both Na+-K+-ATPase and Na+-Ca2+ exchange proteins are involved.

引用

页码：934 / 943

页数：10

共 49 条

[1]

Alpert, Periasamy, Arai, Et al., The regulation of calcium cycling in stressed hearts, Basic Res Cardiol, 87, pp. 71-80, (1992)

[2]

Charlemagne, Orlowski, Oliviero, Et al., Alteration of NaK-ATPase subunit mRNA and protein levels in hypertrophied rat heart, J Biol Chem, 269, pp. 1541-1547, (1994)

[3]

Kent, Rozich, McCollam, Et al., Rapid expression of the Na+-Ca2+ exchanger in response to cardiac pressure overload, Am J Physiol, 265, pp. H1024-H1029, (1993)

[4]

Levitsky, de la Bastie, Schwartz, Lompre, Ca2+-ATPase and function of sarcoplasmic reticulum during cardiac hypertrophy, Am J Physiol, 261, pp. 23-26, (1991)

[5]

Naudin, Oliviero, Rannou, Et al., The density of ryanodine receptors decreases with pressure overload-induced rat cardiac hypertrophy, FEBS Lett, 285, pp. 135-138, (1991)

[6]

Bailey, Houser, Calcium transients in feline left ventricular myocytes with hypertrophy induced by slow progressive pressure overload, J Mol Cell Cardiol, 24, pp. 365-373, (1992)

[7]

Bentivegna, Albin, Kihara, Morgan, Altered calcium handling in left ventricular pressure-overload hypertrophy as detected with aequorin in the isolated perfused ferret heart, Circ Res, 69, 6, pp. 1538-1545, (1991)

[8]

Gwathmey, Morgan, Altered calcium handling in experimental pressure-overload hypertrophy in the ferret, Circ Res, 57, pp. 836-843, (1985)

[9]

Wang, Flemal, Qui, Et al., Ca2+ handling and myofibrillar Ca2+ sensitivity in ferret cardiac myocytes with pressure-overload hypertrophy, Am J Physiol, 267, 3, pp. H918-H924, (1994)

[10]

Beuckelmann, Nabauer, Erdmann, Intracellular calcium handling in isolated ventricular myocytes from patients with terminal heart failure, Circulation, 85, pp. 1046-1055, (1992)

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