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1Department of Physiology II, Nara Medical University, Kashihara 634-8521; and 2Department of Anatomy, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan
Submitted 13 November 2003 ; accepted in final form 19 February 2004
Left ventricular (LV) myocardial slices were isolated from murine hearts (300 µm thick) and were stimulated at 1 Hz without external load. Mean myocardial slice O2 consumption (MVO2) per minute (mMVO2) without stimulation was 0.97 ± 0.14 ml O2·min1·100 g LV1 and mean mMVO2 with stimulation increased to 1.80 ± 0.17 ml O2·min1·100 g LV1 in normal Tyrode solution. Mean
mVO2 (the mMVO2 with stimulation the mMVO2 without stimulation) was 0.83 ± 0.12 ml O2·min1·100 g LV1. There were no differences between mean mMVO2 with and without stimulation in Ca2+-free solution. The increases in extracellular Ca2+ concentrations up to 14.4 mM did not affect the mMVO2 without stimulation but significantly increased the mMVO2 with stimulation up to 140% of control. The
mMVO2 significantly increased up to 190% of the control in a dose-dependent manner. In contrast, the shortening did not increase in a dose-dependent manner. Cyclopiazonic acid (CPA; 30 µM) significantly reduced the
mMVO2 to 0.27 ± 0.06 ml O2·min1·100 g LV1 (35% of control). The combination of 5 mM 2,3-butanedione monoxime (BDM) and 30 µM CPA did not further decrease
mMVO2. Although BDM (35 mM) decreased the
mMVO2 by 2830% of control in a dose-independent manner, 35 mM BDM decreased shortening in a dose-dependent manner. Our results indicate that the
mMVO2 of mouse LV slices during shortening under mechanically unloaded conditions consists of energy expenditure for total Ca2+ handling during excitation-contraction coupling, basal metabolism, but no residual cross-bridge cycling.
excitation-contraction coupling; basal metabolism; free shortening
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