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Titlebook: Role of Nitric Oxide in Sepsis and ARDS; M. P. Fink,Didier Payen Book 1995 Springer-Verlag Berlin Heidelberg 1995 ARDS.Arginin.Edotoxin.Li

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楼主: Philanthropist
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Biochemistry and Synthesis of NO in Sepsis until the 1980s that NO was considered to be more than a toxic atmospheric gas. The aim of this chapter will be to discuss the biochemistry and synthesis of NO, its regulation and the potential cytotoxic and cytoprotective roles in which it is involved during sepsis.
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Effects of Hypoxia on Inducible Nitric Oxide Synthase (iNOS) in Renal Mesangial Cells lipopolysaccharide (LPS), are prolific generators of NO. The importance of examining the iNOS pathway at multiple levels, from induction of messenger ribonucleic acid (mRNA) and iNOS activity to the postsynthetic fate of NO and activation of molecular targets, is explained.
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Blocking the Effects of Nitric Oxide in Septic Shockffects 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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Nitric Oxide as a Mediator in Gram-Positive Sepsissms. Gram-positive bacteria are increasingly being recognized as the cause of septic shock and sepsis syndromes [3]; in most series, they account for 40–50% of cases of bacteremia, and the mortality is at least as high as that seen complicating gram-negative infections.
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Book 1995ributed chapters dealing with cutting-edge science and practical clinical strategies. Numerous tables and charts have been included to aid the reader in understanding this fascinating and important subject.
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0933-6788 have contributed chapters dealing with cutting-edge science and practical clinical strategies. Numerous tables and charts have been included to aid the reader in understanding this fascinating and important subject.978-3-642-79922-8978-3-642-79920-4Series ISSN 0933-6788
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Vascular Smooth Muscle Function under Conditions of Sepsis and Endotoxemiaplegia”. The importance of understanding the mechanisms involved in this vasoplegia and “unrelenting hypotension” [4] lies in the observation that this is a major contributory factor to mortality in both adult [5–8] and pediatric [9] patients with sepsis.
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Inhibition of Nitric Oxide Synthase Activity in Circulatory Shock: Friend or Foe?se (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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