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Table 1 Summary of neurological outcomes in acute focal brain ischemia NBO studies that measure oxidative stress

From: Does normobaric hyperoxia increase oxidative stress in acute ischemic stroke? A critical review of the literature

Model NBO intervention Oxidative stress results Neurological outcome results Ref.
MCAO (2 h) and reperfusion (60 min ) in rats NBO (100 % O2) during MCAO and reperfusion NBO did not increase HO-1 induction and protein carbonyl formation (no significant differences between groups) NBO significantly reduced total infarct volume (70 %) and cortex infarct volume (92 %), but not significantly in the striatum. No significant differences in BBB damage. [12]
MCAO (1,2,3, or 4 h) in rats NBO (100 % O2) during MCAO NBO did not increase markers for O2· generation (Het) (no significant differences between groups) NBO groups improved neurological scores and had significantly smaller infarct volumes after 1,2, and 3 h MCAO [14]
MCAO (90 min) and reperfusion (90 min) in rats dNBO (95 % O2) during MCAO or rNBO during reperfusion dNBO (not rNBO) significantly reduced 8-OHdG production. dNBO and rNBO did not affect O2· generation (Het). NBO during MCAO significantly reduced infarct volume (40 %). NBO during reperfusion reduced infarction volume (15 %: not significant) [17]
MCAO (90 min) and reperfusion (22.5 h) in WT and gp91phox-KO mice NBO (95 % O2) during MCAO NBO significantly inhibited gp91phox expression, NADPH oxidase activity, and MMP-9 induction in WT NBO treatment and gp91phox-KO significantly reduced BBB damage. Inhibition of gp91phox may be an important mechanism underlying NBO-afforded BBB protection [23]
MCAO (90 min) and reperfusion (90 min) in mice dNBO (100 % O2) during MCAO or rNBO (100 %) during reperfusion dNBO significantly decreased levels of 4HNE, NT, 8-OHdG oxidation. No significant differences with rNBO dNBO significantly reduced infarct volume (~50 %) and improved sensorimotor scores. rNBO worsened the ischemic lesion, but no significant difference in sensorimotor scores [27]
BCAO (15 min) and blood pressure (50 mmHg) reduction in rats NBO (100 % O2; 3 h) after BCAO NBO did not lead to enhanced H2O2 or ROS production (no significant differences between groups) No significant differences in caudoputaminal and neocortical damaged neurons score or percent of hippocampal necrotic neurons [32]
MCAO (90 min) and reperfusion (22.5 h) in rats NBO (95 % O2) given during MCAO NBO significantly inhibited gp91phox expression and NADPH oxidase activity NBO significantly reduced MRI ADC lesion volume (37 %) [67]
MCAO (90 min) and reperfusion (22.5 h) in rats iNBO (100 % O2), sNBO, nNBO, or cNBOa iNBO and nNBO groups significantly decreased O2· production (Het) iNBO significantly reduced infarct volume (34 %) equivalent to nNBO. sNBO did not decrease infarct volume and cNBO did not improve protection over iNBO or nNBO [69]
MCAO (90 min) and reperfusion (22.5 h) in rats NBO (100 % O2) given for 2,4 or 8 h 30 min after MCAO NBO (2,4 and 8 h) significantly reduced 8-OHdG and gp91phox production (greatest reduction with 8 h NBO) NBO (2,4 and 8 h) significantly reduced total infarct volume and infarct volume in the cortex and subcortex (8 h NBO offered the greatest efficacy) [70]
MCAO (90 min) and reperfusion (22.5 h) in rats NBO (95 % O2) given during MCAO NBO significantly inhibited gp91phox expression, NADPH oxidase activity, and MMP-9 induction NBO significantly decreased BBB permeability coefficient (MRI) and brain edema [71]
MCAO (90 min) in WT and SOD2-KO mice NBO (100 % O2) (60 min) started 25 min after MCAO NBO significantly decreased O2· generation (Het) in WT mice. NBO does not affect infarct size in SOD2-KO mice and the effect of NBO on infarct size in WT mice was not presented [72]
MCAO (10,30,60 or 90 min) in rats NBO (95 % O2) given during MCAO NBO significantly delayed and attenuated ·NO production (NOx:nitrite plus nitrate) and significantly reduced 3-NT formation NBO significantly decreased total infarct volume, particularly in the cortex, but not significantly in the striatum [73]
  1. MCAO middle cerebral artery occlusion, HO-1 heme oxygenase-1, O 2 · superoxide, Het dihydroethidium, dNBO during MCAO, rNBO during reperfusion, 4HNE 4-hydroxynonenal, NT nitrotyrosine, 8-OHdG 8-hydroxy-2′–deoxyguanosine, BCAO bilateral carotid artery occlusion, WT wild-type, KO knock-out, iNBO Intermittent, sNBO Short, nNBO normal or continuous, cNBO combination, ·NO nitric oxide
  2. a see reference for details