O<sub>2</sub>cost of contractility but not of mechanical energy increases with temperature in canine left ventricle

Mikane, Takeshi; Araki, Junichi; Suzuki, Shunsuke; Mizuno, Ju; Shimizu, Juichiro; Mohri, Satoshi; Matsubara, Hiromi; Hirakawa, Masahisa; Ohe, Tohru; Suga, Hiroyuki

doi:10.1152/ajpheart.1999.277.1.h65

Cited by 23 publications

(40 citation statements)

References 19 publications

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“…A criticism of our myothermic experiments is that they were generally performed in the range 17-27°C (though Q 10 necessarily varies inversely with temperature [64]). Thus we are gratified by the results of a recent study of Mikane et al [115], using their cross-circulated, blood-perfused, isolated dog heart preparation. From 30 to 39°C they found a Q 10 of only 1.14.…”

Section: Modifiers Of Basal Metabolismmentioning

confidence: 94%

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: 94%

Cardiac Basal Metabolism.

Gibbs

Loiselle²

2001

JJP

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“…Data analyses. We analyzed the E max -PVA-VO 2 data by our routine methodology [5,[10][11][12][13][14][15][16][17][18]. That which followed is briefly explained here because we explained them elsewhere [5,[10][11][12][13][14][15][16][17][18].…”

Section: Contractility Index (E Max )mentioning

confidence: 99%

“…Positive inotropism of cardiac cooling decreased the O 2 cost of E max , whereas negative inotropism of cardiac warming increased it at a Q 10 of 2-3 between 30-40°C [17,18]. However, no literature has yet documented a positive inotropism that has an abnormally high O 2 cost of E max .…”

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confidence: 99%

Mechanoenergetics Characterizing Oxygen Wasting Effect of Caffeine in Canine Left Ventricle.

Takasago

Goto

Hata

et al. 2000

JJP

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has a considerable O 2 wasting effect [1,2] and various approaches have elucidated its mechanisms [2][3][4]. However, this O 2 wasting effect remains to be characterized by the E max -PVA-VO 2 relation, which at present seems one of the most powerful integrative frameworks of cardiac mechanoenergetics [5,6]. Here, E max is the end-systolic maximum pressure-volume ratio (or elastance) and serves as an index of contractility reasonably independent of cardiac loading conditions [5][6][7]. PVA is the systolic pressure-volume (P-V ) area that quantitates the total mechanical energy of ventricular contraction [5,6,8]. VO 2 is O 2 consumption by ventricular contraction. The E max -PVA-VO 2 framework is compatible with the Starling law of the heart [9]. In this framework, the O 2 cost of E max serves as a physiologically sound quantitative measure of the O 2 demand for unit increment in E max [5,[10][11][12][13][14][15][16].We have already shown that calcium, catecholamines, digitalis, and phosphodiesterase inhibitors (DPI 201-106, OPC-8212, EMD-53998, milrinone, sulmazole, etc.) have comparable O 2 cost of E max in the normal canine heart [5,10,11,15]. We have also shown that the O 2 cost of E max increases by 50-100% of the control in failing hearts produced by myocardial acidosis [12], postischemic and post-acidotic Key words: Cardiac energetics, E max , myocardial O 2 consumption, pressure-volume area, PVA.Abstract: Caffeine causes a considerable O 2 waste for positive inotropism in myocardium by complex pharmacological mechanisms. However, no quantitative study has yet characterized the mechanoenergetics of caffeine, particularly its O 2 cost of contractility in the E max -PVA-VO 2 framework. Here, E max is an index of ventricular contractility, PVA is a measure of total mechanical energy generated by ventricular contraction, and VO 2 is O 2 consumption of ventricular contraction. The E max -PVA-VO 2 framework proved to be powerful in cardiac mechanoenergetics. We therefore studied the effects of intracoronary caffeine at concentrations lower than 1 mmol/l on left ventricular (LV) E max and VO 2 for excitationcontraction (E-C) coupling in the excised crosscirculated canine heart. We enhanced LV E max by intracoronary infusion of caffeine after ␤-blockade with propranolol and compared this effect with that of calcium. We obtained the relation between LV VO 2 and PVA with E max as a parameter. We then calculated the VO 2 for the E-C coupling by subtracting VO 2 under KCl arrest from the PVA-independent (or zero-PVA) VO 2 and the O 2 cost of E max as the slope of the E-C coupling VO 2 -E max relation. We found that this cost was 40% greater on average for caffeine than for calcium. This result, for the first time, characterized integratively cardiac mechanoenergetics of the O 2 wasting effect of the complex inotropic mechanisms of intracoronary caffeine at concentrations lower than 1 mmol/l in a beating whole heart.

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“…We equalized peak isovolumic LVPs of the regular beats at 36°C and 38°C to that at 33°C by appropriately adjusting LVV with the servo pump to compensate for the negative inotropism of warming [15][16][17][18][19][20][21][22]. This is the major difference of the experimental conditions in the present study from those in the previous one [14].…”

Section: Methodsmentioning

confidence: 99%

“…Thus, the temperature-dependent RF is indepenunchanged despite increasing LV volume (LVV) at normothermia [13], but it decreases with increasing temperature from 33°C to 38°C at a constant LVV [14]. However, increasing temperature simultaneously decreased ventricular contractility and thus peak isovolumic LV pressure (LVP) at a constant LVV because of the negative inotropism of warming [15][16][17][18][19][20][21][22]. Therefore, it remains unknown whether the temperature-dependently decreased LVP at a constant LVV affected the temperature-dependent RF.…”

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Load Independence of Temperature-Dependent Ca2+ Recirculation Fraction in Canine Heart

Mizuno

Mohri

Shimizu

et al. 2004

JJP

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O₂cost of contractility but not of mechanical energy increases with temperature in canine left ventricle

Cited by 23 publications

References 19 publications

Cardiac Basal Metabolism.

Cardiac Basal Metabolism.

Mechanoenergetics Characterizing Oxygen Wasting Effect of Caffeine in Canine Left Ventricle.

Load Independence of Temperature-Dependent Ca2+ Recirculation Fraction in Canine Heart

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O2cost of contractility but not of mechanical energy increases with temperature in canine left ventricle

Cited by 23 publications

References 19 publications

Cardiac Basal Metabolism.

Cardiac Basal Metabolism.

Mechanoenergetics Characterizing Oxygen Wasting Effect of Caffeine in Canine Left Ventricle.

Load Independence of Temperature-Dependent Ca2+ Recirculation Fraction in Canine Heart

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Product

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O₂cost of contractility but not of mechanical energy increases with temperature in canine left ventricle