Effect of Nitrous Oxide on Cerebral Blood Flow in Normal Humans

Field, LM; Dorrance, D. E.; Krzemińska, Emilia; Barsoum, L. Z.

doi:10.1093/bja/70.2.154

Cited by 63 publications

(33 citation statements)

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“…With regard to the effects of nitrous oxide and xenon on cerebral blood flow and metabolism, the information obtained from computed tomography studies suggests that xenon may offer advantages over nitrous oxide in terms of vasoreactivity and circulatory and metabolic stability. Indeed, nitrous oxide can increase cerebral blood flow and metabolism and disrupts cerebral vasoreactivity, 30,31 effects that would contraindicate its use for the treatment of clinical situations associated with pathologic increases in intracranial pressure, such as stroke. In contrast, xenon up to 70-vol% produces no significant changes in cerebral blood flow and metabolism, [32][33][34] and further maintains vasoreactivity.…”

Section: Figure 2 (A) Experimental Protocol For Middle Cerebral Artementioning

confidence: 99%

Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon

Abraini¹

2005

Annals of the New York Academy of Sciences

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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 inhibitors of the NMDA receptor. We briefly review accumulating evidence that nitrous oxide and xenon at subanesthetic concentrations may have potentially neuroprotective and therapeutic properties, with a particular focus on their beneficial effects on ischemia-induced neuronal death and amphetamine-induced sensitization. Nitrous oxide at 75-vol% and xenon up to 70-vol% reduce ischemia-induced neuronal death induced by occlusion of the middle cerebral artery in rodents, and decrease NMDA-induced Ca2+ influx in neuronal cell cultures, a critical event involved in excitotoxicity. Nitrous oxide at 75-vol% and xenon at 50-vol% further reduced amphetamine-induced locomotor sensitization in rodents. However, at a higher concentration of 75-vol%, xenon shows potentially neurotoxic properties and adverse side effects. Because both agents are rapidly eliminated from the body, it is plausible that their administration at appropriate subanesthetic neuroprotective and therapeutic concentrations may not be associated, in contrast with prototypical NMDA receptor antagonists, with adverse side effects and potentially neurotoxicity. Finally, the possible therapeutic implications in humans are discussed.

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Section: Figure 2 (A) Experimental Protocol For Middle Cerebral Artementioning

confidence: 99%

Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon

Abraini¹

2005

Annals of the New York Academy of Sciences

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show abstract

“…With regard to the effects of nitrous oxide and xenon on cerebral blood flow and metabolism, the information obtained from computed tomography studies suggests that xenon may offer advantages over nitrous oxide in terms of vasoreactivity and circulatory and metabolic stability. Indeed, nitrous oxide can increase cerebral blood flow and metabolism and disrupts cerebral vasoreactivity,30,31 effects that would contraindicate its use for the treatment of clinical situations associated with pathologic increases in intracranial pressure, such as stroke. In contrast, xenon up to 70‐vol% produces no significant changes in cerebral blood flow and metabolism,32‐34 and further maintains vasoreactivity 35.…”

Section: Neuroprotective and Adverse Properties Of Nitrous Oxide And mentioning

confidence: 99%

“…Since nitrous oxide and xenon at appropriate equipotent concentrations produce similar effects, nitrous oxide at first sight could appear as an advantageous solution due to the excessive cost of production of xenon. However, under certain conditions, nitrous oxide can increase cerebral blood flow and metabolism and disrupt cerebral vasoreactivity, effects that contraindicate its use for the treatment of clinical situations associated with pathologic increases in intracranial pressure, such as stroke 30,31. In addition, in contrast with the clinical treatments of stroke that typically use treatment periods of 1‐3 days after the patient is admitted,6 the treatment of drug addiction necessitates longer therapeutic interventions that could contraindicate the clinical use of nitrous oxide because of its myelotoxic, neuropathotoxic, and hematotoxic effects—mainly caused by inactivation of vitamin B12 and successfully reversed by appropriate pharmacological treatment—when it is used for long periods of time 51,52.…”

Section: Possible Therapeutic Implications In Humansmentioning

confidence: 99%

Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon

Abraini

David²,

Lemaire

2005

Annals of the New York Academy of Sciences

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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 inhibitors of the NMDA receptor. We briefly review accumulating evidence that nitrous oxide and xenon at subanesthetic concentrations may have potentially neuroprotective and therapeutic properties, with a particular focus on their beneficial effects on ischemia‐induced neuronal death and amphetamine‐induced sensitization. Nitrous oxide at 75‐vol% and xenon up to 70‐vol% reduce ischemia‐induced neuronal death induced by occlusion of the middle cerebral artery in rodents, and decrease NMDA‐induced Ca2+ influx in neuronal cell cultures, a critical event involved in excitotoxicity. Nitrous oxide at 75‐vol% and xenon at 50‐vol% further reduced amphetamine‐induced locomotor sensitization in rodents. However, at a higher concentration of 75‐vol%, xenon shows potentially neurotoxic properties and adverse side effects. Because both agents are rapidly eliminated from the body, it is plausible that their administration at appropriate subanesthetic neuroprotective and therapeutic concentrations may not be associated, in contrast with prototypical NMDA receptor antagonists, with adverse side effects and potentially neurotoxicity. Finally, the possible therapeutic implications in humans are discussed.

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“…The dissociative anesthetic gas nitrous oxide (N 2 O, ‘laughing gas’) is an example of such an agent. N 2 O is believed to achieve its analgesic, sedative and hypnotic effects through the antagonism of N-methyl- D-aspartate (NMDA) receptor mediated activity [11]–[13], electroencephalographically it reduces frontal slow wave activity [14], [15], and metabolically brain activity either increases or remains unchanged during its administration [16], [17]. N 2 O and the other important NMDA receptor antagonist anesthetic, ketamine, are associated with psychoactivation, perceptual distortion, detachment from reality, and are therefore referred to as ‘dissociative’ agents [12], [13], [18].…”

Section: Introductionmentioning

confidence: 99%

Modulation of Functional EEG Networks by the NMDA Antagonist Nitrous Oxide

2013

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Parietal networks are hypothesised to play a central role in the cortical information synthesis that supports conscious experience and behavior. Significant reductions in parietal level functional connectivity have been shown to occur during general anesthesia with propofol and a range of other GABAergic general anesthetic agents. Using two analysis approaches (1) a graph theoretic analysis based on surrogate-corrected zero-lag correlations of scalp EEG, and (2) a global coherence analysis based on the EEG cross-spectrum, we reveal that sedation with the NMDA receptor antagonist nitrous oxide (N2O), an agent that has quite different electroencephalographic effects compared to the inductive general anesthetics, also causes significant alterations in parietal level functional networks, as well as changes in full brain and frontal level networks. A total of 20 subjects underwent N2O inhalation at either 20%, 40% or 60% peak N2O/O2 gas concentration levels. N2O-induced reductions in parietal network level functional connectivity (on the order of 50%) were exclusively detected by utilising a surface Laplacian derivation, suggesting that superficial, smaller spatial scale, cortical networks were most affected. In contrast reductions in frontal network functional connectivity were optimally discriminated using a common-reference derivation (reductions on the order of 10%), indicating that the NMDA antagonist N2O induces spatially coherent and widespread perturbations in frontal activity. Our findings not only give important weight to the idea of agent invariant final network changes underlying drug-induced reductions in consciousness, but also provide significant impetus for the application and development of multiscale functional analyses to systematically characterise the network level cortical effects of NMDA receptor related hypofunction. Future work at the source space level will be needed to verify the consistency between cortical network changes seen at the source level and those presented here at the EEG sensor space level.

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Effect of Nitrous Oxide on Cerebral Blood Flow in Normal Humans

Cited by 63 publications

References 0 publications

Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon

Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon

Potentially Neuroprotective and Therapeutic Properties of Nitrous Oxide and Xenon

Modulation of Functional EEG Networks by the NMDA Antagonist Nitrous Oxide

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