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1 Department of Physiology II, Nara Medical University, Kashihara, Nara, Japan; Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara, Japan
2 Department of Physiology II, Nara Medical University, Kashihara, Nara, Japan
3 Department of Neurology and Neurosurgery, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan
4 Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara, Japan
* To whom correspondence should be addressed. E-mail: mtakaki{at}naramed-u.ac.jp.
We hypothesized that calpain inhibitor-1 protected left ventricular function from ischemic-reperfusion injury by inhibiting the proteolysis of 
-fodrin. To test this hypothesis, we investigated the effect of calpain inhibitor-1 on left ventricular mechanical work and
energetics in the cross-circulated rat hearts underwent 15-min global ischemia and 60-min reperfusion (n=9). After ischemic-reperfusion with calpain inhibitor-1, mean end-systolic pressure at midrange left ventricular volume (ESPmLVV) and systolic pressure-volume area
(PVA) at midrange left ventricular volume (PVAmLVV: a total mechanical energy per beat) were hardly changed, although they were significantly (P<0.01) decreased after ischemic-reperfusion without calpain inhibitor-1. Mean myocardial oxygen consumption per beat (VO2) intercepts
(PVA-independent VO2; VO2 for the total Ca2+ handling in excitation-contraction coupling and basal metabolism) of VO2-PVA linear relations were also unchanged after ischemic-reperfusion with calpain inhibitor-1, although they were significantly (P<0.01) decreased after ischemic-reperfusion without calpain inhibitor-1. There were no significant differences in O2 costs of left ventricular PVA and contractility among the hearts in control (or normal), post ischemic-reperfusion and post ischemic-reperfusion with calpain inhibitor-1. Western blotting of -fodrin and the immunostaining of 150-kD products of -fodrin confirmed that calpain
inhibitor-1 almost completely protected proteolysis of -fodrin. Our results indicate that calpain
inhibitor-1 prevents the heart from ischemic-reperfusion injury associated with the impairment of total calcium handling by directly inhibiting the proteolysis of -fodrin.
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