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    • Is endothelial-nitric-oxide-synthase-derived nitric oxide involved in cardiac hypoxia/reoxygenation-related damage?

      A Rus Ma Peinado S Blanco Ml Del Moral

      Articles Volume 36 Issue 1 March 2011 pp 69-78

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      Permanent link:
      https://www.ias.ac.in/article/fulltext/jbsc/036/01/0069-0078

    • Keywords

       

      Apoptosis; endothelial nitric oxide synthase; hypoxia; L-NIO; nitric oxide; reoxygenation

    • Abstract

       

      Nitric oxide (NO) has been reported to act both as a destructive and a protective agent in the pathogenesis of the injuries that occur during hypoxia/reoxygenation (H/R). It has been suggested that this dual role of NO depends directly on the isoform of NO synthase (NOS) involved. In this work, we investigate the role that NO derived from endothelial NOS (eNOS) plays in cardiac H/R-induced injury.Wistar rats were submitted to H/R (hypoxia for 30 min; reoxygenation of 0 h, 12 h and 5 days), with or without prior treatment using the selective eNOS inhibitor L-NIO (20 mg/kg). Lipid peroxidation, apoptosis and protein nitration, as well as NO production (NOx), were analysed. The results showed that L-NIO administration lowered NOx levels in all the experimental groups. However, no change was found in the lipid peroxidation level, the percentage of apoptotic cells or nitrated protein expression, implying that eNOS-derived NO may not be involved in the injuries occurring during H/R in the heart. We conclude that L-NIO would not be useful in alleviating the adverse effects of cardiac H/R.

    • Author Affiliations

       

      A Rus1 Ma Peinado1 S Blanco1 Ml Del Moral1

      1. Department of Experimental Biology, University of Jaén, Paraje Las Lagunillas s/n, 23071, Jaén, Spain

    • Dates

       
      Published
      March 2011
      Manuscript received
      27 July 2010
      Accepted
      15 November 2010
      Early published
      14 March 2011

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