Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon

  title={Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon},
  author={Jacques H Abraini and Helene David and Marc Lemaire},
  journal={Annals of the New York Academy of Sciences},
Abstract: Despite the beneficial effects of prototypical glutamatergic receptor antagonists in animal models, the pharmacological attempts by the use of such agents have met with very limited clinical success because these compounds produce adverse side effects and possess an intrinsic neurotoxicity at neuroprotective and therapeutic concentrations. Interestingly, nitrous oxide and xenon, which are anesthetic gases with a remarkably safe clinical profile, have been shown to be effective… 

Neuroprotection by nitrous oxide: Facts and evidence*

Experimental evidence is provided that nitrous oxide, which is a cost-efficient and easily available gas, has potentially neuroprotective properties in rodents when given alone at nonanesthetic concentrations.

Neuroprotective effects of xenon: a therapeutic window of opportunity in rats subjected to transient cerebral ischemia

It is shown that xenon, administered at subanesthetic doses, offers global neuroprotection from reduction of neurotransmitter release induced by ischemia, a critical event known to be involved in excitotoxicity, to reduction of subsequent cell injury and neuronal death.

Interactions between Nitrous Oxide and Tissue Plasminogen Activator in a Rat Model of Thromboembolic Stroke

Nitrous oxide should not be considered a good candidate agent for treating acute ischemic stroke compared with xenon, as it increases brain hemorrhages and disruption of the blood–brain barrier.

Morphological Evidence that Xenon Neuroprotects against N‐Methyl‐dl‐Aspartic Acid‐Induced Damage in the Rat Arcuate Nucleus

It is confirmed that in the rat arcuate nucleus NMA can induce a severe neuronal damage that is already marked after 3 h, and Xenon significantly reduced the neuronal damage at all times and can be then regarded as a promising neuroprotectant agent.

XENON in medical area: emphasis on neuroprotection in hypoxia and anesthesia

The neuroprotective effects of xenon and hypothermia cooperate synergistically whether they are applied synchronously or asynchronously, and promise for innovations in medical gas field once further studies are fulfilled and Xenon’s high cost is overcome.

Pressure‐response analysis of anesthetic gases xenon and nitrous oxide on urate oxidase: a crystallographic study

It is shown that Xe and N2O bind to, compete for, and expand the volume of a hydrophobic cavity located just behind the active site of urate oxidase and further inhibit urate oxidation activity, highlighting the mechanisms by which chemically and metabolically inert gases can alter protein function and produce their pharmacological effects.

Xenon is an Inhibitor of Tissue-Plasminogen Activator: Adverse and Beneficial Effects in a Rat Model of Thromboembolic Stroke

It is shown that xenon is a tPA inhibitor, and xenon could be a golden standard for treating acute ischemic stroke if given after tPA-induced reperfusion, with both unique neuroprotective and antiproteolytic (anti-hemorrhaging) properties.

Neuroprotections and mechanisms of inhalational anesthetics against brain ischemia.

The new generation of inhalational anesthetics has been widely used for general anesthesia in both clinical and experimental settings because of their safety, reliability and potency. A



Reduction of Ischemic Brain Damage by Nitrous Oxide and Xenon

  • H. N. DavidF. Léveillé J. Abraini
  • Biology
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2003
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

Combination of Xenon and Isoflurane Produces a Synergistic Protective Effect against Oxygen–Glucose Deprivation Injury in a Neuronal–Glial Co-culture Model

This work studied the neuroprotective effect of the combination of xenon and isoflurane versus oxygen– glucose deprivation (OGD) injury in a neuronal–glial co-culture model and hypothesized that in combination, their efficacy would be enhanced.

Neuroprotective and neurotoxic properties of the 'inert' gas, xenon.

Uniquely amongst anaesthetics with known NMDA receptor antagonist action, xenon exhibits neuroprotective properties without co-existing neurotoxicity.

Effects of Xenon on In Vitro and In Vivo Models of Neuronal Injury

Xenon exerts a concentration-dependent neuroprotective effect at concentrations below which anesthesia is produced in rodents, unlike either nitrous oxide or ketamine, which are devoid of both neurotoxicity and clinically significant adverse hemodynamic properties.

Ketamine potentiates cerebrocortical damage induced by the common anaesthetic agent nitrous oxide in adult rats

When ketamine and N2O were used in combination the neurotoxic reaction was enhanced to a degree much greater than can be explained by simple additivity, and the apparent synergistic interaction was particularly striking when low doses of the agents were combined, the degree of toxic synergism at higher doses being masked by a ceiling effect.

Nitrous oxide (laughing gas) is an NMDA antagonist, neuroprotectant and neurotoxin

It is shown that N2O, at anesthetically-relevant concentrations, inhibits both ionic currents and excitotoxic neurodegeneration mediated through NMDA receptors and, like other NMDA antagonists, produces neurotoxic side effects which can be prevented by drugs that enhance CABAergic inhibition.

Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs.

These findings raise new questions regarding the safety of these agents in the clinical management of neurodegenerative diseases and reinforce concerns about the potential risks associated with illicit use of PCP.

Xenon prevents cellular damage in differentiated PC-12 cells exposed to hypoxia

Replacement of N2 by xenon in such a hypoxic atmosphere resulted in complete protection against cellular damage and prevention of hypoxia-induced dopamine release, demonstrating the outstanding property of xenon to protect neuron-like cells in ahypoxic situation.

The Neuroprotective Effect of Xenon Administration during Transient Middle Cerebral Artery Occlusion in Mice

In this model of transient focal cerebral ischemia, xenon administration improved both functional and histologic outcome and total cerebral infarct volumes were reduced.