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.