Nitrous Oxide "Analgesia": Resemblance to Opiate Action

Ba, Bengtsson; Ngai, S. H.; Finck, A. Donald

doi:10.1126/science.982058

Cited by 176 publications

(33 citation statements)

References 7 publications

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“…We suggest that nitrous oxide, which had been shown to block central sensitisation, 56,57 could have reduced afferent pain input, leading to only a marginal additional effect of DM over placebos. Indeed, Wu et al, 4 6 whose patients underwent general anesthesia for laparoscopic cholecystectomy, still found that providing DM afforded the possibility of reducing the amount of meperidine after having anesthetized their patients with desflurane plus fentanyl and oxygen without nitrous oxide.…”

Section: Patient Self-evaluationmentioning

confidence: 90%

The role of dextromethorphan in pain control

Weinbroum

Rudick

Paret

et al. 2000

Can J Anesth/J Can Anesth

103

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585CAN J ANESTH 2000 / 47: 6 / pp [585][586][587][588][589][590][591][592][593][594][595][596] Purpose: To review the clinical benefits of dextromethorphan (DM) in pain management, describe its neuropharmacological properties.Source: A Medline search was made for experimental and clinical data on DM use from 1967 to date using keywords nociception, acute and chronic pain control, N-methyl-D-aspartate, antagonists, dextromethorphan. Principle findings: The 930 DM citations mostly described its antitussive, metabolic and toxicological aspects, animal studies and its possible role in minimizing post-brain ischemia complications in humans. The use of DM in acute pain revealed eight original studies involving 443 patients, as well as two preliminary reports and our own unpublished data on 513 patients. Most of the 956 patients had general anesthesia. Eight studies (154 patients) and one case report dealt with chronic pain management. This N-methyl-D-aspartate (NMDA) receptor antagonist binds to receptor sites in the spinal cord and central nervous system, thereby blocking the generation of central acute and chronic pain sensations arising from peripheral nociceptive stimuli and enabling reduction in the amount of analgesics required for pain control. DM attenuated the sensation of acute pain at doses of 30-90 mg, without major side effects, and reduced the amount of analgesics in 73% of the postoperative DM-treated patients. Studies in secondary pain models in healthy volunteers and in various types of chronic pain showed DM to be associated with unsatisfactory pain relief.Conclusion: DM attenuates acute pain sensation with tolerable side effects. Its availability in oral form bestow advantages over other NMDA antagonists.Objectif : Passer en revue les bénéfices cliniques du dextrométhorphane (DM) et décrire ses propriétés neuropharmacologiques. Source : Une recherche dans Medline a fourni des données expérimentales et cliniques sur le DM, utilisé de 1967 à aujourd'hui, à l'aide des mots-clés nociception, soulagement de la douleur aiguë et chronique, N-méthyl-D-aspartate, antagonistes, dextrométhorphane.Constatations principales : Les 930 références trouvées décrivent surtout les aspects antitussifs, métaboliques et toxicologiques du DM, les études sur des animaux et le rôle possible dans la réduction des complications de l'ischémie cérébrale chez l'humain. Huit études originales auprès de 443 patients, deux rapports préliminaires et nos propres données non publiées sur 513 patients concernent le soulagement de la douleur aiguë. La majorité des 956 patients ont eu une anesthésie générale. Huit études (154 patients) et une observation portent sur le traitement de la douleur chronique. Cet antagoniste des récepteurs N-méthyl-D-aspartate (NMDA) se fixe sur les sites récepteurs dans la moelle épinière et le système nerveux central. Il empêche ainsi la propagation centrale des sensations de douleurs aiguës et chroniques provenant de stimuli nociceptifs périphériques, et contribue à la réduction de la quantité d'analgés...

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Section: Patient Self-evaluationmentioning

confidence: 90%

The role of dextromethorphan in pain control

Weinbroum

Rudick

Paret

et al. 2000

Can J Anesth/J Can Anesth

103

View full text Add to dashboard Cite

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“…An involvement of endogenous opioid systems in N 2 O-induced analgesia is evidenced by observations that N 2 O antinociception in experimental animals was sensitive to antagonism by naloxone and other opioid receptor blockers (Berkowitz et al, 1976;Quock et al, 1990Quock et al, , 1993. There is also evidence that N 2 O antinociception is secondary to stimulated neuronal release of endogenous opioid peptides (Quock et al, 1985;Zuniga et al, 1987).…”

mentioning

confidence: 99%

Role of Nitric-Oxide Synthase Isoforms in Nitrous Oxide Antinociception in Mice

Ishikawa

Quock²

2003

J Pharmacol Exp Ther

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Exposure of mice to the anesthetic gas N 2 O evokes a prominent antinociceptive effect that is sensitive to antagonism by nonselective nitric-oxide synthase (NOS) inhibitors. The present study was conducted to identify whether a specific NOS isoform is implicated in N 2 O antinociception in mice. In the abdominal constriction test, exposure of mice to 25, 50, and 70% N 2 O resulted in a concentration-dependent antinociceptive effect that persisted for up to 6 min following removal of the mice from the N 2 O atmosphere into room air. This N 2 O antinociceptive effect was antagonized by pretreatment with S-methyl-Lthiocitrulline (SMTC) and higher doses of L-N 5 -(1-iminoethyl)-ornithine (L-NIO), which reportedly inhibit the neuronal and endothelial isoforms of NOS, respectively. Nevertheless, the N 2 O-induced antinociception was unaffected by pretreatment with low doses of either SMTC or L-NIO or by pretreatment with 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT), which selectively inhibits inducible NOS. The s.c. pretreatment with SMTC and L-NIO reduced brain NOS activity in a dose-dependent manner, whereas AMT had no such effect. Moreover, in blood pressure experiments, SMTC increased SBP in doseunrelated fashion, whereas L-NIO showed an appreciably weaker but dose-related increase in SBP. The i.c.v. pretreatment with SMTC also reduced N 2 O antinociception and brain NOS activity without increasing of SBP. These results suggest that it is the neuronal isoform of NOS that is involved in mediation of the antinociceptive effect of N 2 O in the mice.

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“…These findings of this study support the hypothesis that nitrous oxide antinociception in the mouse abdominal constriction test involves the neuronal release of DYN and ME in the spinal cord. Nitrous oxide is an anesthetic gas with analgesic properties that are sensitive to antagonism by the opioid receptor blockers naloxone [1,14,15] and naltrexone [13]. It was suggested from the results of tolerance and cross-tolerance studies that nitrous oxide might act through stimulating the neuronal release of endogenous opioid peptides [2].…”

mentioning

confidence: 99%

Antagonism of Nitrous Oxide Antinociception in Mice by Intrathecally Administered Antisera to Endogenous Opioid Peptides

et al. 2000

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Previously it was demonstrated that nitrous oxide antinociception in the mouse abdominal constriction test is mediated by κ-opioid receptors. Since nitrous oxide is thought to cause the neuronal release of endogenous opioid peptide to stimulate opioid receptors, this study was designed to identify the opioid peptides involved, especially in the spinal cord, by determining whether nitrous oxide antinociception can be differentially inhibited by intrathecally (i.t.) administered antisera to different opioid peptides. Male NIH Swiss mice were pretreated i.t. with rabbit antisera to opioid peptides then exposed 24 h later to one of three different concentrations of nitrous oxide in oxygen. Dose-response curves constructed from the data indicated that the antinociceptive effect of nitrous oxide was significantly antagonized by antisera to various dynorphins (DYNs) and methionine-enkephalin (ME), but not by antiserum to β-endorphin (β-EP). The AD₅₀ values for nitrous oxide antinociception were significantly elevated by antisera to DYNs and ME but not β-EP. These findings of this study support the hypothesis that nitrous oxide antinociception in the mouse abdominal constriction test involves the neuronal release of DYN and ME in the spinal cord.

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Nitrous Oxide "Analgesia": Resemblance to Opiate Action

Cited by 176 publications

References 7 publications

The role of dextromethorphan in pain control

The role of dextromethorphan in pain control

Role of Nitric-Oxide Synthase Isoforms in Nitrous Oxide Antinociception in Mice

Antagonism of Nitrous Oxide Antinociception in Mice by Intrathecally Administered Antisera to Endogenous Opioid Peptides

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