Oxygen consumption and motility of mechanically unloaded myocardial slices

We have recently established a new measurement system of myocardial O2 consumption per min (mVO2) of mechanically unloaded rat left ventricular (LV) slices (Yasuhara et al.: Am. J. Physiol. 270: H1063-H1070, 1996). Using this system, we have revealed that an increment in O2 consumption (delta mVO2) by electrical stimulation primarily represents mVO2 for Ca2+ handling in the excitation-contraction (E-C) coupling, though much smaller than that in the whole heart preparation. The much smaller delta mVO2 in the sliced myocardium than that in the whole heart is due to the much lower frequency of stimulation (60 bpm against 300 bpm). We consider that delta mVO2 does not contain mVO2 for residual crossbridge cycling from the results showing no effect of 2,3-butanedione monoxime on delta mVO2 despite the large decrease in mechanically unloaded contraction, which is expressed by the motility index. We also revealed that mVO2 without stimulation represents basal metabolism. The basal metabolism in rat myocardial slices, which is much higher than in other mammalian hearts, corresponds to that in the rat whole heart preparation. We finally obtained the results showing that sarcoplasmic reticulum (SR) Ca2+ pump blockers, thapsigargin and cyclopiazonic acid, did not reduce basal metabolic mVO2 but both of them reduced delta mVO2 maximally by 50-70% of control and markedly reduced the motility index. We conclude that myocardial O2 consumption (VO2) is composed of VO2 for E-C coupling and basal metabolism and does not contain VO2 for residual crossbridge cycling. Basal metabolic VO2 does not include VO2 for the SR Ca2+ pump, and at least two-thirds of VO2 for E-C coupling represents VO2 for the SR Ca2+ pump.