Mechanical, energetic, and biochemical changes in long-term volume overload of rabbit heart

Gibbs, C. L.; Wendt, Igor R; Kotsanas, George; Young, I. R.

doi:10.1152/ajpheart.1992.262.3.h819

Cited by 19 publications

(23 citation statements)

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“…In long-term volume overload (aortocaval shunt) there was a small but significant increase in basal metabolism [109]. In daunomycin-induced cardiomyopathy, the acute administration of the agent stimulated basal metabolism and seemed to prevent the time-dependent fall [105], but with long-term daunomycin-induced hypertrophy, the basal metabolism was depressed whether assessed polarographically or myothermically (see Fig.…”

Section: Modifiers Of Basal Metabolismmentioning

confidence: 97%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

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The cardiac basal metabolism is the rate of energy expenditure of the quiescent myocardium. It is also called the resting metabolism or the arrested heart metabolism. It has been measured in numerous ways, and in vivo there is good evidence that it accounts for about 1/5 to 1/3 of the total energy flux. The difficulty arises, however, when the heart is stopped because the magnitude of the basal metabolism depends, as blood viscosity, on how and under what physiological condition it is measured. It is possible for the in vivo basal value to fall to less than 1/5 of its original value without cellular damage or to increase to values 5 times greater than its probable in vivo magnitude (i.e., to rise to values in excess of the energy flux of the normally beating heart) by altering the composition of the perfusion medium. We have written on this subject several times [1][2][3], but believe that developments in knowledge now make it possible for us to speculate in a more informed manner. Since several million openheart operations are performed on arrested hearts worldwide each year, it would seem imperative that we understand the cellular mechanisms that can change the magnitude of basal metabolism.A. V. Hill [4] has pointed out that in examining physiological activities, it is necessary to assume a baseline from which some quantity or rate can be measured. If the energy flux produced by the beating heart were very large compared with the energy flux of the arrested heart, baseline ambiguity would be relatively unimportant. But this is not so in regard to the heart; its basal metabolism is high. Within a species, the basal metabolism of cardiac tissue is several-fold higher than the resting metabolism of skeletal muscle and is an order of magnitude greater than the resting metabolism of amphibian skeletal muscle.Species differences are clearly evident in the magnitude of cardiac basal metabolism, and we believe that the major reason for these differences relates to the leakiness of cell membranes, such as those of the sarcolemma and sarcoplasmic reticulum and those of Japanese Journal of Physiology, 51, 399-426, 2001 Key words: whole hearts, isolated preparations, biochemical contributors, modifiers, species difference, temperature, substrate, hypoxia. Abstract:We endeavor to show that the metabolism of the nonbeating heart can vary over an extreme range: from values approximating those measured in the beating heart to values of only a small fraction of normal-perhaps mimicking the situation of nonflow arrest during cardiac bypass surgery. We discuss some of the technical issues that make it difficult to establish the magnitude of basal metabolism in vivo. We consider some of the likely contributors to its magnitude and point out that the biochemical reasons for a sizable fraction of the heart's basal ATP usage remain unresolved. We consider many of the physiological factors that can alter the basal metabolic rate, stressing the importance of substrate supply. We point out that the protective effect of hypothermia ...

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Section: Modifiers Of Basal Metabolismmentioning

confidence: 97%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

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“…Both procedures have been described in longterm overload studies [2,3]. Rabbits were initially anesthetised with i.v.…”

Section: Production Of Hypertrophymentioning

confidence: 99%

“…Recently Gibbs et al [2,3] using right ventricular preparations, have studied the mechanical, energetic, and biochemical changes resulting from a long-term (10-16 weeks) volume overload and a long-term pressure overload of rabbit heart. The volume overload was produced by creating an abdominal aortocaval shunt and the pressure overload by placing a constricting band around the pulmonary artery.…”

Section: Introductionmentioning

confidence: 99%

Mechanical and energetic changes in short-term volume and pressure overload of rabbit heart

et al. 1992

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The mechanical and energetic consequences of a short-term volume overload (STVOL) hypertrophy and short-term pressure overload (STPOL) hypertrophy have been investigated in rabbits and compared with short-term sham-operated controls (STSOC). Hypertrophy was induced either by creating an aortocaval shunt (volume overload) or by banding the pulmonary artery (pressure overload). Suitable papillary muscles were excised from the hearts 8-10 days after the surgical procedure. At 27 degrees C and a stimulus frequency of 1.0 Hz, peak stress development of the STVOL preparations was significantly reduced from the control group, whereas no significant difference in peak stress development was evident between the STPOL and STSOC groups. Surprisingly, the STPOL preparations displayed pulsus alternans after only 8-10 days of inducing the overload. At steady-state conditions, the isometric 10%-90% rise times, the 90%-10% relaxation times, and the 1/2-widths were not significantly different between the treated and control groups. In isotonically contracting muscles working against a range of afterloads, the enthalpy (energy) and work output of the STVOL and STPOL preparations were depressed compared to the STSOC preparations; the differences were statistically significant for the STVOL group. Due to the parallel change in work and enthalpy, the mechanical efficiency was unaltered. A force-length-area (FLA) analysis, analogue of the pressure-volume-area (PVA) analysis, was applied to the isotonic data of this study. The isotonic enthalpy at the various load levels was plotted against the measured FLA and the data were fitted by linear regression. It was evident that the FLA correlated closely with the energy used. The STVOL and STPOL mean total energy:FLA regression lines lay parallel to but were below the STSOC line, signifying a drop in the activation heat, although this reduction did not achieve statistical significance. It is concluded that significant mechanical and energetic changes are evident after a short-term volume overload although earlier work has shown that these differences are absent at the later, compensated stage of hypertrophy. Changes associated with the pressure overload model suggest a disturbance in calcium regulation: this effect is also seen in long-term pressure overload.

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“…The V O 2 -PVA relationship allows quantification of energy conversion efficiency of the contractile machinery (contractile efficiency) and energy use for excitation-contraction (E-C) coupling and basal metabolism (6,34). We found that blockade of endogenous ET-1 in HF produces complex effects on V O 2 through ET A receptor inhibition.…”

mentioning

confidence: 92%

Endothelin receptor blockade has an oxygen-saving effect in Dahl salt-sensitive rats with heart failure

Noguchi

Chen

Bell

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Endothelin receptor blockade has an oxygen-saving effect in Dahl salt-sensitive rats with heart failure. Am J Physiol Heart Circ Physiol 285: H1428-H1434, 2003. First published June 5, 2003 10.1152/ ajpheart.00731.2002The effects of endothelin (ET) receptor blockade on energy utilization in heart failure (HF) are unknown. We administered ET type A (ET A), ET type B (ET B), and ETA/ETB antagonists to isolated hearts from Dahl salt-sensitive (DS) rats with HF and controls. Contractile efficiency was assessed as slope Ϫ1 of myocardial O2 consumption (V O2)-pressure-volume area relation. In HF, ETA and ETA/ETB but not ETB blockade decreased the contractility index (Emax) (Ϫ15 Ϯ 3% and Ϫ17 Ϯ 2%, P Ͻ 0.05), excitationcontraction (E-C) coupling V O2 (Ϫ39 Ϯ 4% and Ϫ37 Ϯ 5%, P Ͻ 0.01), and efficiency (Ϫ15 Ϯ 4% and Ϫ17 Ϯ 2%, P Ͻ 0.05). Despite decreased efficiency, ETA and ETA/ETB blockade decreased total V O2 (Ϫ24 Ϯ 3% and Ϫ22 Ϯ 2%, P Ͻ 0.05). Na ϩ /H ϩ exchanger inhibition decreased Emax and E-C coupling V O2 similar to ETA and ETA/ETB blockade, but did not alter efficiency. In HF, endogenous ET-1 maintains contractility at expense of increased V O2 through ETA receptor activation, likely mediated by Na ϩ /H ϩ exchange.oxygen consumption ACUTELY ADMINISTERED ENDOTHELIN (ET)-1 has positive inotropic effects in normal myocardium (22,27). In contrast, chronic ET-1 inhibition improves cardiac function and prognosis in animal models of heart failure (HF) (23,29,33). Recently, Takeuchi et al. (35) reported that in addition to positive inotropic effects acutely administered exogenous ET-1 increases left ventricular (LV) chemomechanical energy conversion efficiency through ET type A (ET A ) receptor activation in normal rats. The role of endogenous ET-1 in energy utilization in HF, where chronic activation is present, has not been assessed in vitro. Moreover, there are no reports comparing ET A and ET B receptors in this setting.To clarify these issues, we used the myocardial O 2 consumption (V O 2 )-pressure-volume area (PVA) framework to delineate effects of acute ET-1 blockade on mechanoenergetics in isolated, crystalloid-perfused hearts from Dahl salt-sensitive (DS) rats, which develop pressure and volume overload when fed a highsalt (HS) diet (4). The V O 2 -PVA relationship allows quantification of energy conversion efficiency of the contractile machinery (contractile efficiency) and energy use for excitation-contraction (E-C) coupling and basal metabolism (6, 34). We found that blockade of endogenous ET-1 in HF produces complex effects on V O 2 through ET A receptor inhibition. E-C coupling energy saving effects compensate for the energy-wasting effects on the contractile machinery, resulting in net reduction in energy consumption. METHODS Animal ModelAll protocols were reviewed and approved by the Institutional Animal Care and Use Committee of the University of Vermont.Sixty 6-wk-old male DS rats (Taconic Farms, Germantown, NY) were divided into groups receiving a HS (8% NaCl) or low-salt (LS) diet (0.3% NaCl). Com...

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Mechanical, energetic, and biochemical changes in long-term volume overload of rabbit heart

Cited by 19 publications

References 0 publications

Cardiac Basal Metabolism.

Cardiac Basal Metabolism.

Mechanical and energetic changes in short-term volume and pressure overload of rabbit heart

Endothelin receptor blockade has an oxygen-saving effect in Dahl salt-sensitive rats with heart failure

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