BURN-INDUCED NITRIC-OXIDE RELEASE IN HUMANS

Citation
Rl. Gamelli et al., BURN-INDUCED NITRIC-OXIDE RELEASE IN HUMANS, The journal of trauma, injury, infection, and critical care, 39(5), 1995, pp. 869-878
Citations number
51
Categorie Soggetti
Emergency Medicine & Critical Care
Volume
39
Issue
5
Year of publication
1995
Pages
869 - 878
Database
ISI
SICI code
Abstract
Nitric oxide (NO) generation in a series of 20 burn patients was studi ed with a novel anion exchange high-performance liquid chromatographic method for the simultaneous determination of nitrite (NO2-) and nitra te (NO3-), the stable metabolic endproducts of NO. The NO values withi n 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 equa l to 0.03). NO2- values were significantly depressed in both plasma an d urine, whereas NO,values were significantly elevated in contrast to control values (p less than or equal to 0.03), The ratio of NO2-:NO3- was significantly lower for burn patients versus controls in both plas ma and urine (p < 0.01), The NO generation seemed in part to be depend ent on the percentage of total body surface area burn, most dramatical ly elevated in patients with burns of 10 to 40% total body surface are a, 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-:NO3- ratio (0.001) was relatively unchanged, with reflection of a global depression in NO formation with no change in the individu al component release. Burn injury resulted in an increased release/pro duction of NO that in the first postburn week is maximally elevated im mediately postinjury, NO release, although decreased at day 6 relative to the day 1 values, remained elevated into the second week postinjur y when there was evidence for a further increase in NO production, The enhanced NO3- formation may well result from NO reacting with oxygen- free radicals counteracting superoxide anion-induced destruction of ti ssue, thereby potentially functioning as a protectant molecule.