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

Abstract

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.

Glucose Metabolism and Energy Homeostasis in Mouse Hearts Overexpressing Dominant Negative α2 Subunit of AMP-activated Protein Kinase

“…During our ischemic protocol, the heart stops contracting in less than 1 min. Increased ATP depletion in TG hearts under this condition likely reflects increased ATP consumption for noncontractile function, predominantly for maintaining basal metabolism and ion homeostasis (33,34). On this note, we found a slower decline in pH i indicating a reduced accumulation of intracellular H ϩ in TG hearts.…”

“…; n ϭ 7-8 per group. myosin ATPase reaction (33,34). During our ischemic protocol, the heart stops contracting in less than 1 min.…”

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

“…Regression analysis of the relationship between cardiac work (assessed as PVA) and MV O 2 indicated that the decreased efficiency was not due to altered work-dependent MV O 2 (contractile efficiency) but rather to increased work-independent MV O 2 (unloaded MV O 2 ), expressed as an increase in the extrapolated value of the y-intercept of the regression line (26,29). Unloaded MV O 2 is the oxygen cost for nonmechanical work, consisting of the energy expenditure for BM and processes associated with EC coupling (20,48,50). The present study confirms, by direct measurement in mechanically unloaded hearts, that high FA exposure increases unloaded MV O 2 and is due not only to an increase in oxygen cost for BM but also to increased oxygen cost for EC 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).…”

“…Similar to changes seen in diabetic hearts, an acute increase in FA supply to the normal heart also decreases efficiency due to increased work-independent MV O 2 (26,29). This oxygen cost represents the energy cost for nonmechanical purposes in the heart (20,48). The underlying processes leading to the acute and chronic FA-induced increase in workindependent MV O 2 are far from clear.…”