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Am J Physiol Heart Circ Physiol 278: H1008-H1015, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 3, H1008-H1015, March 2000

RAPID COMMUNICATION
Mechanisms of ischemic preconditioning effects on Ca2+ paradox-induced changes in heart

Ken-Ichi Kawabata, Thomas Netticadan, Mitsuru Osada, Kohji Tamura, and Naranjan S. Dhalla

Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6; and Second Department of Internal Medicine Yamanashi Medical University, Yamanashi 409-3898, Japan

The effects of ischemic preconditioning (IP) on changes in cardiac performance and sarcoplasmic reticulum (SR) function due to Ca2+ paradox were investigated. Isolated perfused hearts were subjected to IP (three cycles of 3-min ischemia and 3-min reperfusion) followed by Ca2+-free perfusion and reperfusion (Ca2+ paradox). Perfusion of hearts with Ca2+-free medium for 5 min followed by reperfusion with Ca2+-containing medium for 30 min resulted in a dramatic decrease in the left ventricular (LV) developed pressure and a marked increase in LV end-diastolic pressure. Alterations in cardiac contractile activity due to Ca2+ paradox were associated with depressed SR Ca2+-uptake, Ca2+-pump ATPase, and Ca2+-release activities as well as decreased SR protein contents for Ca2+-pump and Ca2+ channels. All these changes due to Ca2+ paradox were significantly prevented in hearts subjected to IP. The protective effects of IP on Ca2+ paradox changes in cardiac contractile activity as well as SR Ca2+-pump and Ca2+-release activities were lost when the hearts were treated with 8-(p-sulfophenyl)-theophylline, an adenosine receptor antagonist; KN-93, a specific Ca2+/calmodulin-dependent protein kinase II (CaMK II) inhibitor; or chelerythrine chloride, a protein kinase C (PKC) inhibitor. These results indicate that IP rendered cardioprotection by preventing a depression in SR function in Ca2+ paradox hearts. Furthermore, these beneficial effects of IP may partly be mediated by adenosine receptors, PKC, and CaMK II.

ischemic preconditioning; calcium paradox; cardiac function; cardiac sarcoplasmic reticulum


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