JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Abraini, J. H. Articles by Risso, J.-J. Search for Related Content PubMed PubMed Citation Articles by Abraini, J. H. Articles by Risso, J.-J. Related Collections Mechanisms Pharmacology

---

ANESTHETIC PHARMACOLOGY

Gamma-Aminobutyric Acid Neuropharmacological Investigations on Narcosis Produced by Nitrogen, Argon, or Nitrous Oxide

Jacques H. Abraini^*, Badreddine Kriem, Norbert Balon, Jean-Claude Rostain, and Jean-Jacques Risso^,

*UMR CNRS 6551 Mort Neuronale, Neuroprotection, Neurotransmission, Université de Caen, Centre Cyceron; EMI INSERM 0014, Université Henri Poincaré Nancy 1; UPRES EA3280, Université de la Méditerranée, Marseille; and Institut de Médecine Navale du Service de Santé des Armées (IMNSSA), Toulon, France

Address correspondence and reprint requests to Dr. Jacques H. Abraini, Université de Caen, UMR CNRS 6551, Centre Cyceron, BP 5229, Boulevard Henri Becquerel, 14074 Caen Cedex, France. Address e-mail to abraini{at}neuro.unicaen.fr

Inhaled anesthetics, including the gaseous anesthetics nitrous oxide and xenon, are thought to act by interacting directly with ion-channel receptors. In contrast, little is known about the mechanism of action of inert gases that show only narcotic potency at high pressures, such as nitrogen or argon. In the present study, we investigated the effects of selective -aminobutyric acid (GABA) receptor antagonists on narcosis produced by nitrogen, argon, and nitrous oxide. Pretreatment with the competitive GABA_A receptor antagonist gabazine (0.2 nmol) but not the GABA_B receptor antagonist 2-hydroxysaclofen (10 nmol) increased the nitrogen and argon threshold pressure for loss-of-righting-reflex (P < 0.005) but had no effect on nitrous oxide narcosis. Pretreatment with the GABA_A benzodiazepine receptor antagonist flumazenil (5 nmol) also increased the narcosis threshold pressure of argon (P < 0.025). Given that neither 2-hydroxysaclofen, gabazine, nor flumazenil at the doses used induced hyperexcitability, our results support a selective antagonism by gabazine and flumazenil of the narcotic action of nitrogen and argon. Some mechanisms of nitrogen and argon narcotic action might be similar to those of clinical inhaled anesthetics.

IMPLICATIONS: We studied the effects in the rat of -aminobutyric acid (GABA) receptor antagonists on narcosis induced by nitrogen and argon that act only at high pressures. Our results show that the GABA _A receptor may play a significant role, suggesting that some mechanisms might be similar to those of clinical inhaled anesthetics.

This article has been cited by other articles:

				N. Colloc'h, J. Sopkova-de Oliveira Santos, P. Retailleau, D. Vivares, F. Bonnete, B. Langlois d'Estainto, B. Gallois, A. Brisson, J.-J. Risso, M. Lemaire, et al. Protein Crystallography under Xenon and Nitrous Oxide Pressure: Comparison with In Vivo Pharmacology Studies and Implications for the Mechanism of Inhaled Anesthetic Action Biophys. J., January 1, 2007; 92(1): 217 - 224. [Abstract] [Full Text] [PDF]

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999