Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats

Object. 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.