Nitric oxide production is inhibited in trauma patients

Timothy D. Jacob, Juan B. Ochoa, Anthony O. Udekwu, J. Wilkinson, T. Murray, Timothy R. Billiar, Richard L. Simmons, Donald W. Marion, Andrew B. Peitzman*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

64 Scopus citations

Abstract

Elevated levels of nitrates/nitrites, the stable endproducts of nitric oxide (NO), were recently observed in septic patients. In this setting, NO maintains blood flow by vasodilation and inhibition of platelet aggregation. Trauma patients were found to have low plasma levels of nitrates/nitrites, even when they developed sepsis. The current study substantiated that trauma patients have suppressed production of NO; reductions in plasma nitrate/nitrite levels correlated with low urinary excretion of these endproducts. Nitric oxide production was upregulated in trauma patients with clinical infection compared with trauma patients without infection, but was still significantly suppressed compared with nitric oxide production in normal controls. The inability of trauma patients to produce NO may be an important component of the susceptibility of these patients to infection.

Original languageEnglish
Pages (from-to)590-597
Number of pages8
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume35
Issue number4
DOIs
StatePublished - Oct 1993
Externally publishedYes

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