Burn-Induced Nitric Oxide Release in Humans
- 1 November 1995
- journal article
- research article
- Published by Wolters Kluwer Health in The Journal of Trauma: Injury, Infection, and Critical Care
- Vol. 39 (5) , 869-878
- https://doi.org/10.1097/00005373-199511000-00010
Abstract
Nitric oxide (NO) generation in a series of 20 burn patients was studied with a novel anion exchange high-performance liquid chromatographic method for the simultaneous determination of nitrite (NO2 sup -) and nitrate (NO3 sup -), the stable metabolic endproducts of NO. The NO values within our survivor group (n = 17) were significantly altered at days 1, 6, and 12 postburn in contrast to controls (n = 23) (p less than or equal to 0.03). NO2 sup - values were significantly depressed in both plasma and urine, whereas NO3 sup - values were significantly elevated in contrast to control values (p less than or equal to 0.03). The ratio of NO2 sup -:NO3 sup - was significantly lower for burn patients versus controls in both plasma and urine (p < 0.01). The NO generation seemed in part to be dependent on the percentage of total body surface area burn, most dramatically elevated in patients with burns of 10 to 40% total body surface area. In subjects who did not survive beyond 36 hours postinjury because of irreversible shock (n = 3), the production of NO was significantly depressed in contrast to survivors and controls (p < 0.0001). However, the NO2 sup -:NO3 sup - ratio (0.001) was relatively unchanged, with reflection of a global depression in NO formation with no change in the individual component release. Burn injury resulted in an increased release/production of NO that in the first postburn week is maximally elevated immediately postinjury. NO release, although decreased at day 6 relative to the day 1 values, remained elevated into the second week postinjury when there was evidence for a further increase in NO production. The enhanced NO3 sup - formation may well result from NO reacting with oxygen-free radicals counteracting superoxide anion-induced destruction of tissue, thereby potentially functioning as a protectant molecule.Keywords
This publication has 43 references indexed in Scilit:
- Tissue injury caused by deposition of immune complexes is L-arginine dependent.Proceedings of the National Academy of Sciences, 1991
- Biosynthesis and Metabolism of Endothelium-Derived Nitric OxideAnnual Review of Pharmacology and Toxicology, 1990
- Total cavopulmonary connectionThe Journal of Thoracic and Cardiovascular Surgery, 1990
- Nitric oxide: A cytotoxic activated macrophage effector moleculeBiochemical and Biophysical Research Communications, 1988
- Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide.Proceedings of the National Academy of Sciences, 1987
- Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factorNature, 1987
- Macrophage Cytotoxicity: Role for L-Arginine Deiminase and Imino Nitrogen Oxidation to NitriteScience, 1987
- Oxy-Radicals and Related Species: Their Formation, Lifetimes, and ReactionsAnnual Review of Physiology, 1986
- Mechanisms of Nitrogen Dioxide Reactions: Initiation of Lipid Peroxidation and the Production of Nitrous AcidScience, 1981
- The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholineNature, 1980