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Modification of alterations in cardiac function and sarcoplasmic reticulum by vanadate in ischemic-reperfused rat hearts

¹Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada; and ²Department of Medicine, Jikei University, Tokyo, Japan

Submitted 27 February 2005 ; accepted in final form 3 May 2005

To study the cardioprotective effects of vanadate on ischemia-reperfusion (I/R) injury, isolated rat hearts perfused at constant flow were subjected to global ischemia for 30 min followed by reperfusion for 30 min. In this experimental model, I/R markedly decreased ventricular developed pressure and increased end-diastolic pressure. Pretreatment of hearts with 4 µM vanadate attenuated I/R-induced cardiac dysfunction. The reduction in sarcoplasmic reticulum (SR) Ca²⁺ uptake and Ca²⁺ release, as well as SR protein contents for Ca²⁺-pump ATPase and Ca²⁺-release channel, was also prevented by vanadate. Pretreatment of hearts with an antioxidant mixture containing superoxide dismutase + catalase exerted effects similar to those of vanadate in I/R hearts. Postischemic treatment of hearts with vanadate or superoxide dismutase + catalase also had beneficial effects on I/R-induced changes in cardiac performance and SR function. Alterations in cardiac function and SR Ca²⁺ transport due to an oxyradical-generating system (xanthine + xanthine oxidase) or an oxidant (H₂O₂) were attenuated by treatment with vanadate. These results suggest that vanadate may exert beneficial effects on cardiac performance and SR function in I/R hearts because of its antioxidant action.

ischemia-reperfusion; oxidative stress

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				R. B. Singh, V. Elimban, and N. S. Dhalla Differences in ischemia-reperfusion-induced endothelial changes in hearts perfused at constant flow and constant pressure J Appl Physiol, December 1, 2008; 105(6): 1779 - 1787. [Abstract] [Full Text] [PDF]