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Reduction of ischemic brain damage by nitrous oxide and xenon.
J Cereb Blood Flow Metab. 2003 Oct; 23(10):1168-73.JC

Abstract

Neuronal death after ischemia-induced brain damage depends largely upon the activation of the N-methyl-D-aspartate (NMDA) excitatory glutamate receptor that is a target for many putative neuroprotective agents. Whereas the NMDA receptors mediate ischemic brain damage, blocking them is deleterious in humans. Here, the authors investigated whether nitrous oxide or xenon, which are gaseous anesthetics with a remarkably safe clinical profile that have been recently demonstrated as effective inhibitors of the NMDA receptor, may reduce the following: (1) ischemia-induced brain damage in vivo, when given after occlusion of the middle cerebral artery (MCAO), a condition needed to make these potentially neuroprotective agents therapeutically valuable; or (2) NMDA-induced Ca2+ influx in cortical cell cultures, a major critical event involved in excitotoxic neuronal death. The authors have shown that both nitrous oxide at 75 vol% and xenon at 50 vol% reduce ischemic neuronal death in the cortex by 70% and further decrease NMDA-induced Ca2+ influx by 30%. In addition, xenon at 50%, but not nitrous oxide at 75 vol%, further decreases ischemic brain damage in the striatum (a subcortical structure that is known to be resistant to neuroprotective interventions). However, at a higher concentration (75 vol%), xenon exhibits potentially neurotoxic effects. The mechanisms of the neuroprotective and potentially neurotoxic effects of nitrous oxide and xenon, as well as the possible therapeutic implications in humans, are discussed.

Authors+Show Affiliations

Université de Caen-Basse Normandie, Caen, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

14526227

Citation

David, Helene N., et al. "Reduction of Ischemic Brain Damage By Nitrous Oxide and Xenon." Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, vol. 23, no. 10, 2003, pp. 1168-73.
David HN, Leveille F, Chazalviel L, et al. Reduction of ischemic brain damage by nitrous oxide and xenon. J Cereb Blood Flow Metab. 2003;23(10):1168-73.
David, H. N., Leveille, F., Chazalviel, L., MacKenzie, E. T., Buisson, A., Lemaire, M., & Abraini, J. H. (2003). Reduction of ischemic brain damage by nitrous oxide and xenon. Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, 23(10), 1168-73.
David HN, et al. Reduction of Ischemic Brain Damage By Nitrous Oxide and Xenon. J Cereb Blood Flow Metab. 2003;23(10):1168-73. PubMed PMID: 14526227.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reduction of ischemic brain damage by nitrous oxide and xenon. AU - David,Helene N, AU - Leveille,Frederic, AU - Chazalviel,Laurent, AU - MacKenzie,Eric T, AU - Buisson,Alain, AU - Lemaire,Marc, AU - Abraini,Jacques H, PY - 2003/10/4/pubmed PY - 2003/11/13/medline PY - 2003/10/4/entrez SP - 1168 EP - 73 JF - Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism JO - J Cereb Blood Flow Metab VL - 23 IS - 10 N2 - Neuronal death after ischemia-induced brain damage depends largely upon the activation of the N-methyl-D-aspartate (NMDA) excitatory glutamate receptor that is a target for many putative neuroprotective agents. Whereas the NMDA receptors mediate ischemic brain damage, blocking them is deleterious in humans. Here, the authors investigated whether nitrous oxide or xenon, which are gaseous anesthetics with a remarkably safe clinical profile that have been recently demonstrated as effective inhibitors of the NMDA receptor, may reduce the following: (1) ischemia-induced brain damage in vivo, when given after occlusion of the middle cerebral artery (MCAO), a condition needed to make these potentially neuroprotective agents therapeutically valuable; or (2) NMDA-induced Ca2+ influx in cortical cell cultures, a major critical event involved in excitotoxic neuronal death. The authors have shown that both nitrous oxide at 75 vol% and xenon at 50 vol% reduce ischemic neuronal death in the cortex by 70% and further decrease NMDA-induced Ca2+ influx by 30%. In addition, xenon at 50%, but not nitrous oxide at 75 vol%, further decreases ischemic brain damage in the striatum (a subcortical structure that is known to be resistant to neuroprotective interventions). However, at a higher concentration (75 vol%), xenon exhibits potentially neurotoxic effects. The mechanisms of the neuroprotective and potentially neurotoxic effects of nitrous oxide and xenon, as well as the possible therapeutic implications in humans, are discussed. SN - 0271-678X UR - https://www.unboundmedicine.com/medline/citation/14526227/Reduction_of_ischemic_brain_damage_by_nitrous_oxide_and_xenon_ L2 - https://journals.sagepub.com/doi/10.1097/01.WCB.0000087342.31689.18?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -