Titlebook: Shock, Sepsis, and Organ Failure — Nitric Oxide; Fourth Wiggers Berna Günther Schlag,Heinz Redl Conference proceedings 1995 Springer-Verlag

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Septic Shock: A Central Role for Nitric Oxide, pathophysiological vasodilation, hematological abnormalities, and major organ dysfunction. Sepsis affects 300 000–500 000 patients annually in the United States (Parrillo 1989). The incidence of this illness increased by 139% between 1979 and 1987 (Morbidity and Mortality Weekly Report 1988). This

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Inhibition of Nitric Oxide Synthase During Sepsis and Endotoxemia May Be Detrimental,ry excretion of N0. and elevated plasma levels of nitrite and nitrate (N0./ N0.), the stable end-products of NO [1–3]. Results in previous reports suggest that NO may be responsible for hemodynamic and metabolic consequences of sepsis and endotoxemia, and that inhibition of NO synthesis may be benef

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Vasodilators in Sepsis,polysaccharide (endotoxin) by gram-negative bacteria. However, exotoxin of gram-positive bacteria as well as viral and fungal products produce the same clinical picture [2]. Because noninfectious diseases can cause the same inflammatory response seen in infectious sepsis, Bone et al. proposed the te

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The Nitric Oxide Pathway in the Control of Myocardial Function: Role of Cytokines,evere infections. These systemic responses to injury or infection are major causes of morbidity and mortality, despite the effective therapies that are often available to manage the primary causes (Bone 1991).

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,Nitric Oxide Dependent and Independent Effects of Tumor Necrosis Factor-α on Cardiomyocyte Beating ) for the determination of TNFα- and soluble TNF receptor-plasma levels (see Fig. 13) and to Miss Susanne Grill and Miss Petra Ebner for expert technical assistance. This study was supported by the Deutsche Forschungsgemeinschaft (Mu 1010/1–4; Re 714–2/1; Sta 311/2–1).

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Effect of Nitrosylated Albumin in the Isolated Rabbit Heart,etection of S-nitroso compounds, especially S-nitrosylated proteins (Stamler et al. 1991,1992a, b; Keaney et al. 1993) and that of dinitrosyl-ferrous iron complexes with protein-bound and with low molecular weight thiols (Mülsch et al. 1991; Vanin et al. 1993; Busse et al. 1993) have been reported.

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Comments to NO in Trauma,ation of endotoxin in blood, which can either be translocated during hemorrhagic shock or released as a result of live . infusions. Therefore we established two different animal models in baboons. In the acute trauma model a decrease in the flow of the superior mesenteric artery occurs during the hy