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Am J Physiol Heart Circ Physiol 288: H1690-H1698, 2005. First published November 4, 2004; doi:10.1152/ajpheart.00666.2004
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Calpain inhibitor-1 protects the rat heart from ischemia-reperfusion injury: analysis by mechanical work and energetics

Yoshiro Yoshikawa,1,2 Hiroji Hagihara,1,2 Yoshimi Ohga,1 Chikako Nakajima-Takenaka,1 Ken-ya Murata,3 Shigeki Taniguchi,2 and Miyako Takaki1

Departments of 1Physiology II and 2Thoracic-Cardiovascular Surgery, Nara Medical University, Kashihara, Nara; and 3Department of Neurology and Neurosurgery, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan

Submitted 6 July 2004 ; accepted in final form 31 October 2004

We hypothesized that calpain inhibitor-1 protected left ventricular (LV) function from ischemia-reperfusion injury by inhibiting the proteolysis of {alpha}-fodrin. To test this hypothesis, we investigated the effect of calpain inhibitor-1 on LV mechanical work and energetics in the cross-circulated rat hearts that underwent 15-min global ischemia and 60-min reperfusion (n = 9). After ischemia-reperfusion with calpain inhibitor-1, mean end-systolic pressure at midrange LV volume and systolic pressure-volume area (PVA) at midrange LV volume (total mechanical energy per beat) were hardly changed, although they were significantly (P < 0.01) decreased after ischemia-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 ischemia-reperfusion with calpain inhibitor-1, although they were significantly (P < 0.01) decreased after ischemia-reperfusion without calpain inhibitor-1. There were no significant differences in O2 costs of LV PVA and contractility among the hearts in control (or normal) postischemia-reperfusion and postischemia-reperfusion with calpain inhibitor-1. Western blot analysis of {alpha}-fodrin and the immunostaining of 150-kDa products of {alpha}-fodrin confirmed that calpain inhibitor-1 almost completely protected the proteolysis of {alpha}-fodrin. Our results indicate that calpain inhibitor-1 prevents the heart from ischemia-reperfusion injury associated with the impairment of total Ca2+ handling by directly inhibiting the proteolysis of {alpha}-fodrin.

cardiac function; systolic pressure-volume area; oxygen consumption; {alpha}-fodrin


Address for reprint requests and other correspondence: M. Takaki, Dept. of Physiology II, Nara Medical Univ., 840 Shijo-cho, Kashihara, Nara 634-8521, Japan (E-mail: mtakaki{at}naramed-u.ac.jp)




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