Abstract
Nitric oxide (NO) as both a vasodilator and under certain circumstances a cyto-toxic molecule is suggested as one of the critical mediators of severe sepsis and septic shock. Whether NO is really a central molecule in sepsis and whether inhibition/scavenging has more beneficial or detrimental effects are, however, controversial questions with conflicting data. Many studies demonstrate either one or both effects; these have been thoroughly reviewed recently [1].
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Schlag, G., Redl, H., Gasser, H., Khakpour, Z., Davies, J. (1999). Successful Administration of the NO Synthase Inhibitor 546C88 as a Delayed Continuous Infusion in a Baboon Model of Septic Shock. In: Schlag, G., Redl, H. (eds) Shock, Sepsis, and Organ Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-58630-9_2
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DOI: https://doi.org/10.1007/978-3-642-58630-9_2
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