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Dynamic changes in nitric oxide and mitochondrial oxidative stress with site-dependent differential tissue response during anoxic preconditioning in rat heart

Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Mitochondrial Research Group-Frontier Inje Research Science and Technology Project, Cardiovascular and Metabolic Diseases Center, Inje University, Busan, Korea

Submitted 22 November 2006 ; accepted in final form 26 March 2007

In this study, dynamic changes in nitric oxide (NO) and mitochondrial superoxide (O₂^–) were examined during anoxic preconditioning (AP) in rat heart model. AP and anoxia-reoxygenation (A/R) were performed on isolated hearts and single cardiomyocytes. The cellular insult in the form of infarct size and DNA damage were localized and correlated with NO synthases (endothelial and inducible) expression levels. The results showed that endocardium was the most affected region in AP groups, whereas the larger area of infarct was confined to mid- and epicardium in the A/R group. Interestingly, a high-level expression of immunofluorescent NO synthases was restricted to viable areas in the AP. In contrast to the gradual increase in O₂^– level that occurred in the AP group, a sudden massive increase in its level was demonstrated at the onset of reoxygenation in the A/R group. The observed increase in NO production during reoxygenation in the AP group was attenuated by inducible NO synthase inhibitor. The study revealed, on a real-time basis, the role played by preconditioning for modulating NO and O₂^– levels on behalf of cell survival. The results afford a better understanding of cardiac-adapting mechanism during AP and the role of inducible NO synthase in this important phenomenon.

mitochondrial superoxide; endocardium; inducible nitric oxide synthase

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