ArticleBrain research2011
The acute antinociceptive effect of HBO₂ is mediated by a NO-cyclic GMP-PKG-KATP channel pathway in mice.
Article in Brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Hyperbaric oxygen treatment attenuates naloxone-precipitated opioid withdrawal behaviors and alters microglial activity in male and female mice.Scientific reports · 2025Article
- Hydrogen sulfide attenuates diabetic neuropathic pain through NO/cGMP/PKG pathway and μ-opioid receptor.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Role of spinal GABA receptors in the acute antinociceptive response of mice to hyperbaric oxygen.Brain research · 2018Article
- The NO-cGMP-PKG signal transduction pathway is involved in the analgesic effect of early hyperbaric oxygen treatment of neuropathic pain.The journal of headache and pain · 2017Article
- The acute antinociceptive effect of hyperbaric oxygen is not accompanied by an increase in markers of oxidative stress.Life sciences · 2014Article
- Involvement of spinal cord opioid mechanisms in the acute antinociceptive effect of hyperbaric oxygen in mice.Brain research · 2013Article
- Involvement of brain opioid receptors in the anti-allodynic effect of hyperbaric oxygen in rats with sciatic nerve crush-induced neuropathic pain.Brain research · 2013Article
- An anxiolytic-like effect of hyperbaric oxygen in the mouse light/dark exploration test.Life sciences · 2012Article
- Successful Treatment of Lower Limb Complex Regional Pain Syndrome following Three Weeks of Hyperbaric Oxygen Therapy.Pain research & managementArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Previous research has found that hyperbaric oxygen (HBO(2)) produces an acute antinociceptive effect that is dependent on nitric oxide (NO). The present study was undertaken to determine whether HBO(2)-induced acute antinociception might involve a NO-cyclic GMP-protein kinase G-ATP-sensitive potassium (K(ATP)) channel pathway. Male NIH Swiss mice were subjected to a 5-min HBO(2) treatment (100% oxygen at 3.5 absolute atmospheres) and antinociception was assessed over the next 6 min still under HBO(2) 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 HBO(2)-induced acute antinociception in a dose-dependent manner. These findings suggest that HBO(2)-induced acute antinociception might be due to activation of a NO-cyclic GMP-protein kinase G-K(ATP) channel pathway.
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Registered trials
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