Research has demonstrated that hyperbaric oxygen (HBO2) treatment produced relief of both acute and chronic pain in patients and animal models. However, the mechanism of HBO2 antinociceptive effect is still elusive. Based on our earlier findings that implicate NO in the acute antinociceptive effect of HBO2, the purpose of this study was to ascertain whether HBO2-induced antinociception in a chronic neuropathic pain model is likewise dependent on NO. Neuropathic pain was induced in male Sprague Dawley rats by four injections of paclitaxel (1.0 mg/kg, i.p.). Twenty-four hours after the last paclitaxel injection, rats were treated for one day or four consecutive days with 60-min HBO2 at 3.5 atmospheres absolute (ATA). Two days before HBO2 treatment, some groups of rats were implanted with Alzet® osmotic minipumps that continuously infused a selective inhibitor of neuronal NO synthase (nNOS) into the lateral cerebral ventricle for 7 days. Mechanical and cold allodynia were assessed every other day, using electronic von Frey and acetone assays, respectively. Rats in the paclitaxel control group exhibited a mechanical or cold allodynia that was significantly reversed by one HBO2 treatment for mechanical allodynia and four HBO2 treatments for cold allodynic. In rats treated with the nNOS inhibitor, the effects of HBO2 were nullified in the mechanical allodynia test but unaffected in the cold allodynia test. In summary, these results demonstrate that the antiallodynic effect of HBO2 in two different pain tests is dependent on NO in the CNS.

Keywords: Antiallodynia; Hyperbaric oxygen; Neuropathic pain; Nitric oxide synthase; Paclitaxel.