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Preconditioning Decreases Ischemia/Reperfusion-Induced Peroxynitrite Formation

https://doi.org/10.1006/bbrc.2001.5308Get rights and content

Abstract

The role for peroxynitrite (ONOO) in the mechanism of preconditioning is not known. Therefore, we studied effects of preconditioning and subsequent ischemia/reperfusion on myocardial ONOO formation in isolated rat hearts. Hearts were subjected to a preconditioning protocol (three intermittent periods of global ischemia/reperfusion of 5 min duration each) followed by a test ischemia/reperfusion (30 min global ischemia and 15 min reperfusion). When compared to nonpreconditioned controls, preceding preconditioning improved postischemic cardiac performance and significantly decreased test ischemia/reperfusion-induced formation of free nitrotyrosine measured in the perfusate as a marker for cardiac endogenous ONOO formation. During preconditioning, however, the first period of ischemia/reperfusion increased nitrotyrosine formation, which was attenuated after the third period of ischemia/reperfusion. We conclude that classic preconditioning inhibits ischemia/reperfusion-induced cardiac formation of ONOO and that subsequent periods of ischemia/reperfusion result in a gradual attenuation of ischemia/reperfusion-induced ONOO generation. This mechanism might be involved in ischemic adaptation of the heart.

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    As exogenous ONOO− may not properly reflect the effect of endogenous ONOO− formation, we have recently measured endogenous ONOO− formation during preconditioning induced by three brief cycles ischemia and reperfusion and also during subsequent test ischemia–reperfusion in isolated working rat hearts to clarify the possible contribution of endogenous ONOO− to ischemic preconditioning. When test ischemia and reperfusion was preceded by preconditioning, ONOO− formation was markedly attenuated upon reperfusion [9]. We have also found that the first brief period of ischemia significantly enhanced endogenous ONOO− formation upon the first brief period of reperfusion, which was significantly reduced after subsequent cycles of brief ischemia–reperfusion periods [9].

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To whom correspondence should be addressed at Cardiovascular Research Group, Department of Biochemistry, University of Szeged, Faculty of Medicine, Dóm tér 9, Szeged, Hungary, H-6720. Fax: (+36) 62 545 097. E-mail: [email protected].

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