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Anesthesia

Xenon has been used as a general anesthetic, but it is more expensive than conventional anesthetics.

Xenon interacts with many different receptors and ion channels, and like many theoretically multi-modal inhalation anesthetics, these interactions are likely complementary. Xenon is a high-affinity glycine-site NMDA receptor antagonist. However, xenon is different from certain other NMDA receptor antagonists in that it is not neurotoxic and it inhibits the neurotoxicity of ketamine and nitrous oxide (N O), while actually producing neuroprotective effects. Unlike ketamine and nitrous oxide, xenon does not stimulate a dopamine efflux in the nucleus accumbens.

Like nitrous oxide and cyclopropane, xenon activates the two-pore domain potassium channel TREK-1. A related channel TASK-3 also implicated in the actions of inhalation anesthetics is insensitive to xenon. Xenon inhibits nicotinic acetylcholine α4β2 receptors which contribute to spinally mediated analgesia. Xenon is an effective inhibitor of plasma membrane Ca ATPase. Xenon inhibits Ca ATPase by binding to a hydrophobic pore within the enzyme and preventing the enzyme from assuming active conformations.

Xenon is a competitive inhibitor of the serotonin 5-HT receptor. While neither anesthetic nor antinociceptive, this reduces anesthesia-emergent nausea and vomiting.

Xenon has a minimum alveolar concentration (MAC) of 72% at age 40, making it 44% more potent than N O as an anesthetic. Thus, it can be used with oxygen in concentrations that have a lower risk of hypoxia. Unlike nitrous oxide, xenon is not a greenhouse gas and is viewed as environmentally friendly. Though recycled in modern systems, xenon vented to the atmosphere is only returning to its original source, without environmental impact.