title: Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats.
abstract: OBJECTIVE
  In the current study, the authors examined the effects of hyperbaric O2 (HBO) following fluid-percussion brain injury and its implications on brain tissue oxygenation (PO2) and O2 consumption (VO2) and mitochondrial function (redox potential).
  
  
  METHODS
  Cerebral tissue PO2 was measured following induction of a lateral fluid-percussion brain injury in rats. Hyperbaric O2 treatment (100% O2 at 1.5 ata) significantly increased brain tissue PO2 in both injured and sham-injured animals. For VO2 and redox potential experiments, animals were treated using 30% O2 or HBO therapy for 1 or 4 hours (that is, 4 hours 30% O2 or 1 hour HBO and 3 hours 100% O2). Microrespirometer measurements of VO2 demonstrated significant increases following HBO treatment in both injured and sham-injured animals when compared with animals that underwent 30% O2 treatment. Mitochondrial redox potential, as measured by Alamar blue fluorescence, demonstrated injury-induced reductions at 1 hour postinjury. These reductions were partially reversed at 4 hours postinjury in animals treated with 30% O2 and completely reversed at 4 hours postinjury in animals on HBO therapy when compared with animals treated for only 1 hour.
  
  
  CONCLUSIONS
  Analysis of data in the current study demonstrates that HBO significantly increases brain tissue PO2 after injury. Nonetheless, treatment with HBO was insufficient to overcome injury-induced reductions in mitochondrial redox potential at 1 hour postinjury but was able to restore redox potential by 4 hours postinjury. Furthermore, HBO induced an increase in VO2 in both injured and sham-injured animals. Taken together, these data demonstrate that mitochondrial function is depressed by injury and that the recovery of aerobic metabolic function may be enhanced by treatment with HBO.
authors.affiliation: Department of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA.
authors.forename: Wilson P
authors.initials: WP
authors.lastname: Daugherty
authors.forename: Joseph E
authors.initials: JE
authors.lastname: Levasseur
authors.forename: Dong
authors.initials: D
authors.lastname: Sun
authors.forename: Gaylan L
authors.initials: GL
authors.lastname: Rockswold
authors.forename: M Ross
authors.initials: MR
authors.lastname: Bullock
mesh_terms: D000818:Animals; D001924:Brain Concussion / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology; D002540:Cerebral Cortex / Q000293:injuries / Q000503:physiopathology; D004292:Dominance, Cerebral / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology*; D006931:Hyperbaric Oxygenation; D008297:Male; D008928:Mitochondria / Q000502:physiology*; D010084:Oxidation-Reduction; D010092:Oximetry; D010101:Oxygen Consumption / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley