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PubMed · 9443363

Nitric oxide and sepsis.

A Holzmann
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Abstract

The ability of NO to control microcirculatory blood flow, maintain vascular integrity, and act as an antiinflammatory mediator appears to be dependent on endothelial-derived NO. The function of excess NO production by iNOS in sepsis and septic shock is unclear but iNOS-derived NO may contribute to systemic hypotension. The use of more specific inhibitors for iNOS will help to define the role of iNOS in sepsis. Modulation of the pulmonary NO-cGMP signal transduction system following LPS treatment results in hyporesponsiveness to inhaled NO and impaired pulmonary vascular response to vasodilators, suggesting potential mechanisms of the pulmonary dysregulation observed in sepsis.

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Administration, InhalationAdultAnimalsChildHumansNitric OxideNitric Oxide SynthasePulmonary CirculationSepsisJournal ArticleReview

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A Holzmann. 1997. Nitric oxide and sepsis.. https://pubmed.ncbi.nlm.nih.gov/9443363/

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