Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats.
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.
Daugherty
Wilson P
WP
Department of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA.
Levasseur
Joseph E
JE
Sun
Dong
D
Rockswold
Gaylan L
GL
Bullock
M Ross
MR
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