Hyperbaric oxygen therapy ameliorates local brain metabolism, brain edema and inflammatory response in a blast-induced traumatic brain injury model in rabbits

Neurochem Res. 2014 May;39(5):950-60. doi: 10.1007/s11064-014-1292-4. Epub 2014 Mar 30.


Many studies suggest that hyperbaric oxygen therapy (HBOT) can provide some clinically curative effects on blast-induced traumatic brain injury (bTBI). The specific mechanism by which this occurs still remains unknown, and no standardized time or course of hyperbaric oxygen treatment is currently used. In this study, bTBI was produced by paper detonators equivalent to 600 mg of TNT exploding at 6.5 cm vertical to the rabbit's head. HBO (100% O2 at 2.0 absolute atmospheres) was used once, 12 h after injury. Magnetic resonance spectroscopy was performed to investigate the impact of HBOT on the metabolism of local injured nerves in brain tissue. We also examined blood-brain barrier (BBB) integrity, brain water content, apoptotic factors, and some inflammatory mediators. Our results demonstrate that hyperbaric oxygen could confer neuroprotection and improve prognosis after explosive injury by promoting the metabolism of local neurons, inhibiting brain edema, protecting BBB integrity, decreasing cell apoptosis, and inhibiting the inflammatory response. Furthermore, timely intervention within 1 week after injury might be more conducive to improving the prognosis of patients with bTBI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood-Brain Barrier
  • Brain / metabolism
  • Brain Edema / prevention & control
  • Brain Injuries / metabolism*
  • Brain Injuries / pathology
  • Caspase 3 / biosynthesis
  • Encephalitis / prevention & control*
  • Hyperbaric Oxygenation
  • Interleukin-8 / biosynthesis
  • Male
  • Rabbits
  • Tumor Necrosis Factor-alpha / biosynthesis


  • Interleukin-8
  • Tumor Necrosis Factor-alpha
  • Caspase 3