Amino acid stimulation of oxygen and substrate utilization by cardiac myocytes.

Burns, Alvin C.; Reddy, William J.

doi:10.1152/ajpendo.1978.235.5.e461

Cited by 22 publications

(27 citation statements)

References 13 publications

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“…The appeal of this explanation, first proferred by Gibbs [2], is enhanced by the observation of an inverse relationship between the rate of turnover of cardiac proteins and body size across species [8]-a relationship that mimics the inverse dependence of cardiac basal heat rate, per se, and body size across species (see section III). Early attempts to test this putative explanation, by providing amino acids in either the coronary perfusate of the in situ dog heart [28] or in the bathing medium superfusing isolated rat papillary muscles [64] proved negative-a surprising result given that amino acids had already been shown to stimulate oxygen utilization by cardiac myocytes in vitro [198].…”

Section: Modifiers Of Basal Metabolismmentioning

confidence: 99%

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: 99%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

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“…It is possible that there are other ion pumps consuming energy and, in particular, the energy flux needed for intracellular calcium homeostasis may be important, even though variations in extracellular calcium have little effect on basal metabolism. Another factor (Gibbs, 1978) is the fraction of the basal metabolism needed for amino acid transport and protein synthesis and degradation (Chapman and Millward et al, 1975;Everett et al, 1977;Banos et al, 1978;Earl et al, 1978;Burns and Reddy, 1978;Schreiber et al, 1977). Gamble et al (1970) report an average value for total mV0 2 of 9.1 ml 0 2 /min per 100 g at 100 mm Hg left ventricular pressure which compares favorably with our value of 9.2 ml/min per 100 g; a lower range of values (4.9-8.6) was reported in unanesthetized resting dogs by Gregg et al (1965).…”

Section: Basal Metabolismmentioning

confidence: 99%

Oxygen consumption of the nonworking and potassium chloride-arrested dog heart.

Gibbs¹,

Papadoyannis²,

Drake³

et al. 1980

Circulation Research

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SUMMARY In 21 dogs on cardiopulmonary bypass with ventricles kept empty, the mean beating but nonworking myocardial oxygen consumption (mVO 2 ) was 3.8 ml/min per 100 g at a heart rate of 158 beats/min. After subsequent potassium chloride arrest, the basal mVOs was 1.74 ml/min per 100 g. To compare these values with the working situation, we measured mVOj in these hearts before instituting bypass when the heart rate averaged 179 beats/min and arterial pressure averaged 108 mm Hg; mVOj was 9.2 ml/min per 100 g. Atrioventricular dissociation was induced in five beating, nonworking hearts; electrical pacing at increasing heart rates produced a linear increase in mVO2. Extrapolation to zero heart rate yielded a value of 1.24 ml/min per 100 g, which was not significantly different from the KC1 arrest value of 1.25 ml/min per 100 g in these same hearts. THE BASAL OXYGEN consumption of cardiac tissue is higher than that of skeletal muscle. Different groups of experiments, using a variety of techniques to induce cardiac arrest, have measured the basal metabolism in several species of animals (for reviews, see Lochner et al., 1968;Gibbs, 1978). There is a fairly wide scatter among the different estimates, presumably as a result of technique and species differences. It is desirable to measure the basal metabolism accurately so that the real energy cost of a single cardiac contraction can be determined. To calculate this value, the basal metabolism must be subtracted from the total metabolism of the working heart.In the present investigation a cardiopulmonary bypass technique was used so that the oxygen consumption of arrested blood-perfused hearts could be followed in vivo for long periods of time (40 minutes and more). The per beat oxygen cost of (1) the beating working heart and (2) the beating nonworking heart was determined. We know of no other experiments on the in situ blood-perfused heart in which basal metabolism has been studied in this way.

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“…The human heart uses large amounts of amino acids (AAs) as regulators of both myocardium protein turnover [ 1 , 2 , 3 ] and energy metabolism [ 4 , 5 , 6 , 7 , 8 ], but uses few AAs as substrates for direct energy production [ 6 ]. The heart’s reliance on AAs increases during heart failure (HF) because of high myocardium anabolic activity and cardiomyocyte energy shortage [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

“…Even in early HF, in which energy deficiency occurs, there are fewer intermediary metabolites, whereas cardiomyocyte content in AA aspartic acid increases [ 13 ]. These AA serve physiologically to stimulate mitochondrial energy production under anaerobic conditions as well as contributing to replenishing the TCA cycle [ 6 , 7 , 8 ], thus assuming an important pro-energy role.…”

Section: Introductionmentioning

confidence: 99%

Plasma Amino Acid Abnormalities in Chronic Heart Failure. Mechanisms, Potential Risks and Targets in Human Myocardium Metabolism

et al. 2017

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The goal of this study was to measure arterial amino acid levels in patients with chronic heart failure (CHF), and relate them to left ventricular function and disease severity. Amino acids (AAs) play a crucial role for heart protein-energy metabolism. In heart failure, arterial AAs, which are the major determinant of AA uptake by the myocardium, are rarely measured. Forty-one subjects with clinically stable CHF (New York Heart Association (NYHA) class II to IV) were analyzed. After overnight fasting, blood samples from the radial artery were taken to measure AA concentrations. Calorie (KcalI), protein-, fat-, carbohydrate-intake, resting energy expenditure (REE), total daily energy expenditure (REE × 1.3), and cardiac right catheterization variables were all measured. Eight matched controls were compared for all measurements, with the exception of cardiac catheterization. Compared with controls, CHF patients had reduced arterial AA levels, of which both their number and reduced rates are related to Heart Failure (HF) severity. Arterial aspartic acid correlated with stroke volume index (r = 0.6263; p < 0.0001) and cardiac index (r = 0.4243; p = 0.0028). The value of arterial aspartic acid (µmol/L) multiplied by the cardiac index was associated with left ventricular ejection fraction (r = 0.3765; p = 0.0076). All NYHA groups had adequate protein intake (≥1.1 g/kg/day) and inadequate calorie intake (KcalI < REE × 1.3) was found only in class IV patients. This study showed that CHF patients had reduced arterial AA levels directly related to clinical disease severity and left ventricular dysfunction.

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Amino acid stimulation of oxygen and substrate utilization by cardiac myocytes.

Cited by 22 publications

References 13 publications

Cardiac Basal Metabolism.

Cardiac Basal Metabolism.

Oxygen consumption of the nonworking and potassium chloride-arrested dog heart.

Plasma Amino Acid Abnormalities in Chronic Heart Failure. Mechanisms, Potential Risks and Targets in Human Myocardium Metabolism

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