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Inhibition of Nitric Oxide Synthase Activity in Circulatory Shock: Friend or Foe?

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Role of Nitric Oxide in Sepsis and ADRS

Part of the book series: Update in Intensive Care and Emergency Medicine ((UICM,volume 24))

Abstract

Nitric oxide (NO) is a recently discovered autacoid, which is produced by a hitherto unrecognized enzymatic pathway in many mammalian cells. Thus, it is not surprising that NO has many diverse biological functions in the cardiovascular, nervous and immune system [l].The biological activity of NO was first described by Furchgott and Zawadski in 1980 [2] as a labile, vasodilator substance released by endothelial cells in response to acetylcholine (and other endothelium-dependent vasodilators), and called “endothelium-de- rived relaxing factor (EDRF)”. We know today that the formation of NO by the vascular endothelium accounts for the biological activity of EDRF [3,4]. NO is produced from the guanidino nitrogen group of L-arginine by NO synthase (NOS). Once produced, NO diffuses to adjacent cells and activates soluble guanylyl cyclase by binding to the iron on its heme component. The subsequent rise in intracellular cyclic GMP mediates many, but not all, of the biological properties of NO [1].

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Thiemermann, C. (1995). Inhibition of Nitric Oxide Synthase Activity in Circulatory Shock: Friend or Foe?. In: Fink, M.P., Payen, D. (eds) Role of Nitric Oxide in Sepsis and ADRS. Update in Intensive Care and Emergency Medicine, vol 24. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79920-4_13

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  • DOI: https://doi.org/10.1007/978-3-642-79920-4_13

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-79922-8

  • Online ISBN: 978-3-642-79920-4

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