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Blocking the Effects of Nitric Oxide in Septic Shock

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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))

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Abstract

That isolated vessels and organs and intact organisms markedly increase nitric oxide (NO) release during septic challenge has been amply demonstrated in both animal and human studies. Many experimental protocols using competitive antagonists of L-arginine, the natural precursor of NO, have been performed in vitro, in vivo, and in clinical pilot trials. NO production can be inhibited by several analogs of L-arginine, such as NG-monome- thyl-L-arginine (L-NMMA), Nw-nitro-L-arginine (L-NNA), NG-nitro-L- arginine-methyl ester (L-NAME) and Nw-amino-L-arginine (L-NAA). Methylene blue can be also used to block the effects of NO mediated by the formation of cyclic guanosine monophosphate (cGMP) (Table 1). Trials with these agents have documented the role of NO in the development of vasodilation, hyporesponsiveness to catecholamines, and myocardial depression associated with severe sepsis.

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Vincent, J.L., Preiser, J.G., Zhang, H. (1995). Blocking the Effects of Nitric Oxide in Septic Shock. 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_16

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