Abstract:

Objective To investigate the effects of hyperbaric oxygen (HBO) on mitochondrial function of brain tissues and cognitive function after fluid-percussion injury in rats. Methods SD rats were divided into model group and sham injury group, and fluid-percussion injury was achieved in each rat of model group, which were subdivided into low concentration O₂ treatment group (n=23), high concentration O₂ treatment group (n=24) and HBO treatment group (n=23) according to different ways of O₂ treatment. Rats in sham injury group (n=22) received the same operations with model group, while did not experience fluid-percussion injury, and were treated as low concentration O₂ treatment group. After O₂ treatment, high performance liquid chromatography was employed to detect cortical adenosine triphosphate (ATP) levels, flow cytometry was used to determine mitochondrial reactive oxygen species (ROS) production of brain tissues, and hippocampal neuron counting was performed with Nissl staining. Morris water maze test was adopted to record escape latency, and cognitive function 11 to 15 d after brain injury was evaluated. Results ATP levels of brain tissues in HBO treatment group and high concentration O₂ treatment group were similar to that in sham injury group (P>0.05), and were significantly higher than that of low concentration O₂ treatment group (P<0.05).  Hippocampal neuron counting in CA2/3 and hilus regions in HBO treatment group was significantly higher than that in low concentration O₂ treatment group and high concentration O₂ treatment group (P<0.05). There was no significant difference in mitochondrial ROS production of brain tissues among groups (P>0.05). In Morris water maze test, the escape latency of HBO treatment group was significantly shorter than those of low concentration O₂ treatment group and high concentration O₂ treatment group (P<0.05). Conclusion HBO can maintain brain mitochondrial ATP synthesis for rats with fluidpercussion injury.  Moreover, HBO can improve cognitive function and reduce hippocampal neuron loss after injury.

Key words: traumatic brain injury, hyperbaric oxygen, adenosine triphosphate, hippocampal neuron, cognitive function