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Inducible Nitric Oxide Synthase in Cardiac Adaptation to Ischemia

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Part of the book series: Progress in Experimental Cardiology ((PREC,volume 6))

Summary

Cardiac ischaemia/reperfusion is well known as a disease of the myocytes, it is now clear that reactive oxygen species and their intermediates in conjunction with increased nitric oxide (NO) production during and after ischemia determine the second window of protection. However, regulatory mechanisms of NO modulation during ischaemia/reperfusion are poorly understood. Assuming that increased expression of NO synthases (NOS) could be involved in mediation of cardioprotective effect of preconditioning, we preconditioned cultured neonatal rat cardiocytes with hypoxia, 10εM norepinephrine, or 1εM H2O2. Immunohistochemical assay of an inducible NOS isoform (NOS2) revealed that norepinephrine, hypoxia and H2O2 enhanced the expression of NOS2 in cardiomyocytes, both along contractile fibers and in a cytoplasmic granular component, apparently in mitochondria. Inhibition of NOS2 expression or NOS2 activity abolished the protective preconditioning effect of hypoxia treatment. Hence, NO is implicated as a trigger in this model of preconditioning via activation of inducible NOS isoform. These data provide evidence that an increased NO generation due to induction of inducible NOS, following ischaemia/reperfusion, might be associated with increased myocardial tolerance to infarction.

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Correspondence to Ján Slezák M.D., Ph.D., D.Sc. .

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© 2003 Springer Science+Business Media New York

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Slezák, J. et al. (2003). Inducible Nitric Oxide Synthase in Cardiac Adaptation to Ischemia. In: Dhalla, N.S., Takeda, N., Singh, M., Lukas, A. (eds) Myocardial Ischemia and Preconditioning. Progress in Experimental Cardiology, vol 6. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0355-2_9

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  • DOI: https://doi.org/10.1007/978-1-4615-0355-2_9

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-5036-1

  • Online ISBN: 978-1-4615-0355-2

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