AbstractHyperbaric oxygen (HBO2) therapy is reported to cause pain relief in several conditions of chronicpain. A single 60-min session of HBO2 treatment produced a prolonged antinociceptive effect inmice that persisted for 90 min after cessation of treatment. The HBO2-induced antinociception wassignificantly attenuated by pretreatment prior to HBO2 exposure with the opioid antagonistnaltrexone, the non-specific nitric oxide synthase (NOS)-inhibitor NG-nitro-L-arginine methyl ester(L-NAME) and the selective neuronal NOS-inhibitor S-methyl-L-thiocitrulline (SMTC) but not theselective endothelial NOS-inhibitor N5-(1-iminoethyl)-L-ornithine (L-NIO). The antinociceptionwas also significantly reduced by central pretreatment with a rabbit antiserum against dynorphin1-13 but not by rabbit antisera against either β-endorphin or methionine-enkephalin. The prolonged antinociceptive effect at 90 min after HBO2-induced treatment was also significantly attenuated by naltrexone but not L-NAME administered 60 min following HBO2 treatment but priorto nociceptive testing. These findings indicate that the antinociception that persists for 90 min after HBO2 exposure is mediated by nitric oxide (NO) and opioid mechanisms but that the NO involvement is critical during the HBO2 treatment and not at the time of nociceptive testing. These results are consistent with the concept that HBO2 may induce an NO-dependent release of opioid peptide to cause a long-acting antinociceptive effect.
Categories: Medical clinic, Rheumatology