AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 281: H1286-H1294, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 3, H1286-H1294, September 2001

Rat cardiac contractile dysfunction induced by Ca2+ overload: possible link to the proteolysis of alpha -fodrin

Tsuyoshi Tsuji2, Yoshimi Ohga1, Yoshiro Yoshikawa4, Susumu Sakata1, Takehisa Abe2, Nobuoki Tabayashi2, Shuichi Kobayashi2, Hisaharu Kohzuki1, Ken-Ichi Yoshida3, Hiroyuki Suga4, Soichiro Kitamura4, Shigeki Taniguchi2, and Miyako Takaki1

1 Department of Physiology II and 2 Department of Surgery III, Nara Medical University, Kashihara, Nara 634-8521; 3 Department of Legal Medicine, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033; and 4 National Cardiovascular Center, Suita, Osaka 565-8565, Japan

The aim of the present study was to examine the mechanisms of Ca2+ overload-induced contractile dysfunction in rat hearts independent of ischemia and acidosis. Experiments were performed on 30 excised cross-circulated rat heart preparations. After hearts were exposed to high Ca2+, there was a contractile failure associated with a parallel downward shift of the linear relation between myocardial O2 consumption per beat and systolic pressure-volume area (index of a total mechanical energy per beat) in left ventricles from all seven hearts that underwent the protocol. This result suggested a decrease in O2 consumption for total Ca2+ handling in excitation-contraction coupling. In the hearts that underwent the high Ca2+ protocol and had contractile failure, we found marked proteolysis of a cytoskeleton protein, alpha -fodrin, whereas other proteins were unaffected. A calpain inhibitor suppressed the contractile failure by high Ca2+, the decrease in O2 consumption for total Ca2+ handling, and membrane alpha -fodrin degradation. We conclude that the exposure to high Ca2+ may induce contractile dysfunction possibly by suppressing total Ca2+ handling in excitation-contraction coupling and degradation of membrane alpha -fodrin via activation of calpain.

excitation-contraction coupling; oxygen consumption


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