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1 Department of Physiology II, Nara Medical University, Kashihara, Nara, Japan
2 Department of Anatomy, School of Medicine University of Occupational and Environmental Health, Kitakyushu, Fukuoka, Japan
* To whom correspondence should be addressed. E-mail: mtakaki{at}naramed-u.ac.jp.
Left ventricular (LV) myocardial slices were isolated from murine hearts (300-µm thick) and were stimulated at 1Hz without external load. Mean myocardial slice oxygen consumption per minute (mVO2) without stimulation was 0.97 ± 0.14 ml 0>2.min-1.100 g LV-1 and mean mVO2 with stimulation increased to 1.80 ± 0.17 ml O2.min-1.100 g LV-1 in normal Tyrode solution. Mean delta mVO2 (=the mVO2 with stimulation - the mVO2 without stimulation) was 0.83 ± 0.12 ml O2.min-1.100 g LV-1. There were no differences between mean mVO2 with and without stimulation in Ca2+ free solution. The increases in extracellular Ca2+ concentrations up to 14.4 mM did not affect the mVO2 without stimulation, but significantly increased the mVO2 with stimulation up to 140% of control. The delta mVO2 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 delta mVO2 to 0.27 ± 0.06 ml O2.min-1.100 g LV-1 (35% of control). The combination of 5 mM 2,3-butanedione monoxime (BDM)and 30 µM CPA did not further decrease delta mVO2. Although BDM (3-5 mM) decreased the delta mVO2 by 28-30% of control in a dose-independent manner, 3-5 mM BDM decreased shortening in a dose-dependent manner. Our results indicate that the delta mVO2 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 crossbridge cycling.
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