Cardiac Basal Metabolism.

Abstract

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 ...

Increased O2 consumption in excitation–contraction coupling in hypertrophied rat heart slices related to increased Na+–Ca2+ exchange activity

“…The basal metabolic VO 2 of the whole heart measured by arresting it with KCl (0.03 mM) was 24.3 llO 2 min -1 g -1 (resting VO 2 ; 8.1 mW g -1 or 2.43 mlO 2 min -1 100 g -1 ) [32,33]. These data are in good agreement with the present results and those from the Alpert and Gibbs laboratories in regard to the activation or tension-independent heat [34].…”

Effects of BDM, [Ca2+]o, and temperature on the dynamic stiffness of quiescent cardiac trabeculae from rat

“…Common experimental conditions are 0.5 mM Ca 2ϩ and room temperature. However, when right ventricular trabeculae from rat are subjected to such experimental conditions, spontaneous, asynchronized "waves" of contractile movement, commonly called "writhing," are reported (7,13,21,41). In trabeculae that were deemed to be viable, raising the temperature to 25°C significantly reduced the degree of writhing (7,21 ] i (and, hence, the degree of cross-bridge cycling and resting tension) is higher at lower temperatures in nominally quiescent cardiac muscle tissue.…”

“…The two [Ca 2ϩ ] o were selected to emulate the low level commonly used during mechanical studies of passive myocardium (0.5 mM) and the physiological level for rat (1.25 mM) (4). The two temperatures where chosen to reflect room temperature (ϳ20°C) and a just-sufficient increase (to 26°C) to allow the sarcoplasmic reticulum Ca 2ϩ pump [Q 10 ϭ 3.3 in this temperature range (42)] to reduce intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) to the point at which signs of sarcomere "spontaneous contractile waves" (7,13,41) are abolished.…”

Chronic and acute exposure of mouse hearts to fatty acids increases oxygen cost of excitation-contraction coupling

“…Accordingly, MV O2 measured under this condition is defined as the oxygen cost of basal metabolism (MV O2BM). The calculated difference between the measured unloaded MV O2 obtained in unloaded retrograde mode (MV O2unloaded) and MV O2BM was used to obtain the oxygen cost of EC coupling (MV O2ECC) (2,7,19,20).…”