title: Effect of short periods of normobaric hyperoxia on local brain tissue oxygenation and cerebrospinal fluid oxidative stress markers in severe traumatic brain injury.
abstract: Preliminary evidence suggests local brain tissue oxygenation (PbtO(2)) values of <or=15 mm Hg following severe traumatic brain injury (TBI) represent brain tissue hypoxia. Accordingly, many neurotrauma units attempt to maintain PbtO(2) >or=20 mm Hg to avoid hypoxia. This study tested the impact of a short (2 h) trial of normobaric hyperoxia on measures of oxidative stress. We hypothesized this treatment would positively affect cerebral oxygenation but negatively affect the cellular environment via oxidative stress mechanisms. Cerebrospinal fluid (CSF) was serially assessed in 11 adults (9 male, 2 female), aged 26 +/- 1.8 years with severe TBI (Glasgow Coma Scale score, 6 +/- 1.4) before, during, and after a FiO(2) = 1.0 challenge for markers of oxidative stress, including lipid peroxidation (F(2)-isoprostane [ELISA]), protein oxidation (protein sulfhydryl [fluorescence]), and antioxidant defenses (total antioxidant reserve (AOR) [chemiluminescence] and glutathione [fluorescence]). Physiological parameters [PbtO(2), arterial oxygen content (PaO(2)), intracranial pressure (ICP), mean arterial pressure (MAP), and cerebral perfusion pressure (CPP)] were assessed at the same time points. Mean (+/-SD) PbtO(2) and PaO(2) levels significantly changed for each time point. Oxidative stress markers, antioxidant reserve defenses, and ICP, MAP, and CPP did not significantly change for any time period. These preliminary findings suggest that brief periods of normobaric hyperoxia do not produce oxidative stress and/or change antioxidant reserves in CSF. Additional studies are required to examine extended periods of normobaric hyperoxia in a larger sample.
authors.affiliation: Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, PA 15213, USA. puccioam@upmc.edu
authors.forename: Ava M
authors.initials: AM
authors.lastname: Puccio
authors.forename: Leslie A
authors.initials: LA
authors.lastname: Hoffman
authors.forename: Hülya
authors.initials: H
authors.lastname: Bayir
authors.forename: Thomas G
authors.initials: TG
authors.lastname: Zullo
authors.forename: Michael
authors.initials: M
authors.lastname: Fischer
authors.forename: Joseph
authors.initials: J
authors.lastname: Darby
authors.forename: Sheila
authors.initials: S
authors.lastname: Alexander
authors.forename: C Edward
authors.initials: CE
authors.lastname: Dixon
authors.forename: David O
authors.initials: DO
authors.lastname: Okonkwo
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Kochanek
mesh_terms: D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000378:metabolism / Q000628:therapy*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015600:Glasgow Coma Scale; D006801:Humans; D006931:Hyperbaric Oxygenation / Q000379:methods*; D018496:Hyperoxia / Q000378:metabolism*; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress
chemical_list: D000975:Antioxidants; D015415:Biomarkers