The acute antinociceptive effect of HBO2 is mediated by a NO–cyclic GMP–PKG–KATP channel pathway in mice

Previous research has found that hyperbaric oxygen (HBO2) produces an acute antinociceptive effect that is dependent on nitric oxide (NO). The present study was undertaken to determine whether HBO2-induced acute antinociception might involve a NO–cyclic GMP–protein kinase G–ATP-sensitive potassium (KATP) channel pathway. Male NIH Swiss mice were subjected to a 5-min HBO2 treatment (100% oxygen at 3.5 absolute atmospheres) and antinociception was assessed over the next 6 min still under HBO2 using the acetic acid abdominal constriction test. Pretreatment with 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3-oxide (carboxy-PTIO, an NO scavenger), 1H-[1,2,4]-oxadiazolo-[4,3-a]quinoxalin-1-one) (a soluble guanylyl cyclase-inhibitor, Rp-8-(4-chlorophenylthio)-guanosine-3′,5′-cyclic monophosphorothioate (a protein kinase G-inhibitor) or glibenclamide (an ATP-sensitive potassium channel-inhibitor) all led to antagonism of the HBO2-induced acute antinociception in a dose-dependent manner. These findings suggest that HBO2-induced acute antinociception might be due to activation of a NO–cyclic GMP–protein kinase G–KATP channel pathway.

Research Highlights
► Hyperbaric oxygen (HBO2) induces antinociception in the mouse abdominal constriction test.
► HBO2 antinociception depends on NO, cyclic GMP and PKG.
► There is also involvement of ATP-sensitive potassium channels in HBO2 antinociception.