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1 Deprtment of Physiology II, Nara Medical University, Kashihara, Nara, Japan; Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara, Japan
2 Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara, Japan
3 Deprtment of Physiology II, Nara Medical University, Kashihara, Nara, Japan
4 Department of Neurology and Neurosurgery, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan
* To whom correspondence should be addressed. E-mail: mtakaki{at}naramed-u.ac.jp.
We have recently reported that exposure of rat hearts to high Ca2+ produces a Ca2+-overload induced contractile failure in rat hearts which was associated with proteolysis of 
-fodrin. We hypothesized that contractile failure after ischemic-reperfusion (IR) is similar to that after high Ca2+ infusion. To test this hypothesis, we investigated left ventricular (LV) mechanical work and energetics in the cross-circulated rat hearts which were subjected to 15-min global ischemia and 60-min reperfusion. Sixty minutes after IR, mean systolic pressure-volume area (PVA; a total mechanical energy per beat) at midrange LV volume mLVV)(PVAmLVV) was significantly decreased from 5.89±1.55 to 3.83±1.16 mmHg.ml.beat-1.g-1 (n=6). Mean myocardial oxygen consumption per beat (VO2)intercept of VO2-PVA linear relation was significantly decreased from 0.21±0.05 to 0.15±0.03 µlO2.beat-1.g-1 without change in its slope. Initial 30-min reperfusion with a Na+/Ca2+ exchanger (NCX) inhibitor, KB-R7943 (KBR; 10 µmol/L) significantly reduced the decrease in mean PVAmLVV and VO2 intercept (n=6). Although VO2 for the Ca2+ handling was finally decreased, it transiently but significantly increased from the control for 10-15 min after IR. This increase in VO2 for the Ca2+handling was completely blocked by KBR, suggesting an inhibition of reverse mode NCX by KBR. -fodrin proteolysis which was significantly increased after IR, was also significantly reduced by KBR. Our study shows that the contractile failure after IR is similar to that after high Ca2+ infusion, although the contribution of reverse mode NCX to the contractile failure is different. An inhibition of reverse mode NCX during initial reperfusion protects the heart against reperfusion injury.
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