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==== Anesthesia ==== Xenon has been used as a [[general anesthetic]], but it is more expensive than conventional anesthetics.<ref>{{cite journal | last1 = Neice | first1 = A. E. | last2 = Zornow | first2 = M. H. | title = Xenon anaesthesia for all, or only a select few? | journal = Anaesthesia | year = 2016 | volume = 71 | issue = 11 | pages = 1259β72 | doi = 10.1111/anae.13569 | pmid = 27530275 | doi-access = free }}</ref> 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]].<ref name="nmda">{{cite journal | title = Competitive inhibition at the glycine site of the N-methyl-D-aspartate receptor mediates xenon neuroprotection against hypoxia-ischemia | journal = Anesthesiology | pmid = 20124979 | year = 2010 | last1 = Banks | first1 = P. | last2 = Franks | first2 = N. P. | last3 = Dickinson | first3 = R. | volume = 112 | issue = 3 | pages = 614β22 | doi = 10.1097/ALN.0b013e3181cea398 | doi-access = free }}</ref> However, xenon is different from certain other NMDA receptor antagonists in that it is not [[neurotoxicity|neurotoxic]] and it inhibits the neurotoxicity of [[ketamine]] and [[nitrous oxide]] (N<sub>2</sub>O), while actually producing [[neuroprotection|neuroprotective effects]].<ref>{{cite journal | title = Neuroprotective and neurotoxic properties of the 'inert' gas, xenon | journal = British Journal of Anaesthesia | pmid = 12393773 | year = 2002 | last1 = Ma | first1 = D. | last2 = Wilhelm | first2 = S. | last3 = Maze | first3 = M. | last4 = Franks | first4 = N. P. | volume = 89 | issue = 5 | pages = 739β46 | doi = 10.1093/bja/89.5.739 | doi-access = free }}</ref><ref>{{cite journal | title = Xenon inhibits but N<sub>2</sub>O enhances ketamine-induced c-Fos expression in the rat posterior cingulate and retrosplenial cortices | journal = Anesthesia & Analgesia | pmid = 11159233 | year = 2001 | last1 = Nagata | first1 = A. | last2 = Nakao Si | first2 = S. | last3 = Nishizawa | first3 = N. | last4 = Masuzawa | first4 = M. | last5 = Inada | first5 = T. | last6 = Murao | first6 = K. | last7 = Miyamoto | first7 = E. | last8 = Shingu | first8 = K. | s2cid = 15167421 | volume = 92 | issue = 2 | pages = 362β368 | doi = 10.1213/00000539-200102000-00016 | doi-access = free }}</ref> Unlike ketamine and nitrous oxide, xenon does not stimulate a dopamine efflux in the [[nucleus accumbens]].<ref>{{cite journal | title = The differential effects of nitrous oxide and xenon on extracellular dopamine levels in the rat nucleus accumbens: a microdialysis study | journal = [[Anesthesia & Analgesia]] | pmid = 17122223 | year = 2006 | last1 = Sakamoto | first1 = S. | last2 = Nakao | first2 = S. | last3 = Masuzawa | first3 = M. | last4 = Inada | first4 = T. | last5 = Maze | first5 = M. | last6 = Franks | first6 = N. P. | last7 = Shingu | first7 = K. | s2cid = 1882085 | volume = 103 | issue = 6 | pages = 1459β63 | doi = 10.1213/01.ane.0000247792.03959.f1 }}</ref> Like nitrous oxide and [[cyclopropane]], xenon activates the two-pore domain potassium channel [[KCNK2|TREK-1]]. A related channel [[KCNK9|TASK-3]] also implicated in the actions of inhalation anesthetics is insensitive to xenon.<ref>{{cite journal | title = Two-pore-domain K<sup>+</sup> channels are a novel target for the anesthetic gases xenon, nitrous oxide, and cyclopropane | journal = Molecular Pharmacology | pmid = 14742687 | year = 2004 | last1 = Gruss | first1 = M. | last2 = Bushell | first2 = T. J. | last3 = Bright | first3 = D. P. | last4 = Lieb | first4 = W. R. | last5 = Mathie | first5 = A. | last6 = Franks | first6 = N. P. | s2cid = 7762447 | volume = 65 | issue = 2 | pages = 443β52 | doi = 10.1124/mol.65.2.443 }}</ref> Xenon inhibits nicotinic acetylcholine [[Alpha-4 beta-2 nicotinic receptor|Ξ±4Ξ²2]] receptors which contribute to spinally mediated analgesia.<ref>{{cite journal | title = Effects of gaseous anesthetics nitrous oxide and xenon on ligand-gated ion channels. Comparison with isoflurane and ethanol | journal = Anesthesiology | pmid = 11020766 | year = 2000 | last1 = Yamakura | first1 = T. | last2 = Harris | first2 = R. A. | s2cid = 4684919 | volume = 93 | issue = 4 | pages = 1095β101 | doi = 10.1097/00000542-200010000-00034 | doi-access = free }}</ref><ref>{{cite journal | title = Tonic inhibitory role of Ξ±4Ξ²2 subtype of nicotinic acetylcholine receptors on nociceptive transmission in the spinal cord in mice | journal = Pain | pmid = 16781069 | year = 2006 | last1 = Rashid | first1 = M. H. | last2 = Furue | first2 = H. | last3 = Yoshimura | first3 = M. | last4 = Ueda | first4 = H. | s2cid = 53151557 | volume = 125 | issue = 1β2 | pages = 125β35 | doi = 10.1016/j.pain.2006.05.011 }}</ref> Xenon is an effective inhibitor of [[Plasma membrane Ca2+ ATPase|plasma membrane Ca<sup>2+</sup> ATPase]]. Xenon inhibits Ca<sup>2+</sup> ATPase by binding to a hydrophobic pore within the enzyme and preventing the enzyme from assuming active conformations.<ref>{{cite journal | first1 = Maria M. | last1 = Lopez | last2 = Kosk-Kosicka | first2 = Danuta | title = How Do Volatile Anesthetics Inhibit Ca<sup>2+</sup>-ATPases? | journal = [[The Journal of Biological Chemistry]] | year = 1995 | doi = 10.1074/jbc.270.47.28239 | pmid = 7499320 | volume = 270 | issue = 47 | pages = 28239β245 | doi-access = free }}</ref> Xenon is a competitive inhibitor of the [[serotonin]] [[5-HT3 receptor|5-HT<sub>3</sub> receptor]]. While neither anesthetic nor antinociceptive, this reduces anesthesia-emergent nausea and vomiting.<ref>{{cite journal | title = The diverse actions of volatile and gaseous anesthetics on human-cloned 5-hydroxytryptamine<sup>3</sup> receptors expressed in ''Xenopus'' oocytes | journal = Anesthesiology | pmid = 11873047 | year = 2002 | last1 = Suzuki | first1 = T. | last2 = Koyama | first2 = H. | last3 = Sugimoto | first3 = M. | last4 = Uchida | first4 = I. | last5 = Mashimo | first5 = T. | s2cid = 6705116 | volume = 96 | issue = 3 | pages = 699β704 | doi = 10.1097/00000542-200203000-00028 | doi-access = free }}</ref> Xenon has a [[minimum alveolar concentration]] (MAC) of 72% at age 40, making it 44% more potent than N<sub>2</sub>O as an anesthetic.<ref>{{cite journal | last1 = Nickalls | first1 = R.W.D. | last2 = Mapleson | first2 = W.W. | title = Age-related iso-MAC charts for isoflurane, sevoflurane and desflurane in man | journal = British Journal of Anaesthesia | date = August 2003 | volume = 91 | issue = 2 | pages = 170β74 | doi = 10.1093/bja/aeg132 | pmid = 12878613 | doi-access = free }}</ref> Thus, it can be used with oxygen in concentrations that have a lower risk of [[Hypoxia (medical)|hypoxia]]. Unlike nitrous oxide, xenon is not a [[greenhouse gas]] and is viewed as [[environmentally friendly]].<ref name="Goto2003">{{Cite journal | last = Goto | first = T. | author2 = Nakata Y | author3 = Morita S | s2cid = 19119058 | title = Will xenon be a stranger or a friend?: the cost, benefit, and future of xenon anesthesia | journal = Anesthesiology | volume = 98 | issue = 1 | pages = 1β2 | year = 2003 | pmid = 12502969 | doi = 10.1097/00000542-200301000-00002 | doi-access = free }}</ref> Though recycled in modern systems, xenon vented to the atmosphere is only returning to its original source, without environmental impact.
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