Multicenter Randomized Comparison of the Efficacy and Safety of Xenon and Isoflurane in Patients Undergoing Elective Surgery

Rossaint, Rolf; Reyle-Hahn, M.; Esch, Jochen Schulte am; Scholz, Jens; Scherpereel, P; Vallet, B.; Giunta, Francesco; Turco, M.; Erdmann, W.; Tenbrinck, R.; Hammerle, A. F.; Nägele, Peter

doi:10.1097/00000542-200301000-00005

Cited by 189 publications

(134 citation statements)

References 15 publications

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“…Xenon is also attractive in this role because of its lack of chemical reactivity and lack of clinical side effects (Dingley et al, 2001;Marx et al, 1997;Preckel et al, 2004;Rossaint et al, 2003), rapid reversibility, and lack of fetotoxicity (Burov et al, 2002;Lane et al, 1980). A radioisotope of Xe (Xe 133 ) has been used in neonates by injecting Xe 133 dissolved in 1 ml of water and counting the distribution of radioactivity as a measure of blood flow.…”

Section: Introductionmentioning

confidence: 99%

Cooling Combined with Immediate or Delayed Xenon Inhalation Provides Equivalent Long-Term Neuroprotection after Neonatal Hypoxia—Ischemia

Thoresen

Hobbs

Wood

et al. 2009

J Cereb Blood Flow Metab

151

117

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Hypothermia (HT) improves outcome after neonatal hypoxia-ischemia. Combination therapy may extend neuroprotection. The noble anesthetic gas xenon (Xe) has an excellent safety profile. We have shown earlier that 3 h of 50% Xe plus HT (321C) additively gives more protection (72%) than either alone (HT = 31.1%, Xe = 10.2%). Factors limiting clinical use include high-cost and specialist administration requirements. Thus, combinations of 1 h of 50% Xe were administered concurrently for either the first (1 h Immediate Xe) or last (1 h Delayed Xe) of 3 h of posthypoxic-ischemic HT as compared with 3 h of 50%Xe/HT to investigate how brief Xe exposure with a delay would affect efficacy. An established neonatal rat hypoxia-ischemia model was used. Serial functional neurologic testing into adulthood was performed, followed by neuropathological examination. Xenon with HT was more effective with longer Xe duration (3 h versus 1 h) (P = 0.015). However, 1 h Xe/3 h HT resulted in better neuroprotection than 3 h HT alone (P = 0.03), this significant effect was also present with 1 h Xe after a 2-h delay. One (immediate or with a delay) or 3 h Xe also significantly improved motor function (P = 0.024). Females had significantly better motor scores than males, but no sex-dependent difference in pathology results. The neuroprotection of short, delayed Xe treatment would allow transport to specialist facilities to receive Xe.

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Section: Introductionmentioning

confidence: 99%

Cooling Combined with Immediate or Delayed Xenon Inhalation Provides Equivalent Long-Term Neuroprotection after Neonatal Hypoxia—Ischemia

Thoresen

Hobbs

Wood

et al. 2009

J Cereb Blood Flow Metab

151

117

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“…25 Additional advantages in human anesthesia include; ease of administration, rapid onset of action, and rapid recovery. 29,30 Since xenon is exceedingly scarce, difficult to extract in large quantities, and, consequently, very costly, progress in making it commercially available as a general anesthetic has been impeded.…”

Section: Discussionmentioning

confidence: 99%

Potential of xenon to induce or to protect against neuroapoptosis in the developing mouse brain

Cattano

Williamson

Fukui

et al. 2008

Can J Anesth/J Can Anesth

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reports of original investigation 429 CAN J ANESTH 55: 7 www.cja-jca.org July, 2008 Purpose: Drugs that suppress neuronal activity, including all general anesthetics that have been tested thus far (ketamine, midazolam, isoflurane, propofol, and a cocktail of midazolam, nitrous oxide and isoflurane), trigger neuroapoptosis in the developing rodent brain. Combinations of nitrous oxide and isoflurane, or ketamine and propofol, cause more severe neuroapoptosis than any single agent by itself, which suggests a positive correlation between increased levels of anesthesia and increased severity of neuroapoptosis. In contrast, there is evidence that the rare gas, xenon, which has anesthetic properties, protects against isoflurane-induced neuroapoptosis in the infant rat brain, while not inducing neuroapoptosis by itself. The present study was undertaken to evaluate the potential of xenon to induce neuroapoptosis or to protect against neuroapoptosis induced by isoflurane in the infant mouse brain. Methods:Seven-day-old C57BL/6 mice were exposed to one of four conditions: air (control); 0.75% isoflurane; 70% xenon; or 0.75% isoflurane + 70% xenon for four hours. For histopathological evaluation of the brains, all pups were euthanized two hours later using activated caspase-3 immunohistochemical staining to detect apoptotic neurons. Under each condition, quantitative assessment of the number of apoptotic neurons in the cerebral cortex (CC) and in the caudate/putamen (C/P) was performed by unbiased stereology. Results:The combination of xenon + isoflurane produced a deeper level of anesthesia than either agent alone. Both xenon alone (p < 0.003 in CC; p < 0.02 in C/P) and isoflurane alone (p < 0.001 in both CC and C/P) induced a significant increase in neuroapoptosis compared to controls. The neuroapoptotic response to isoflurane was substantially more robust than the response to xenon. When xenon was administered together with isoflurane, the apoptotic response was reduced to a level lower than that for isoflurane alone (p < 0.01 in CP; marginally non-significant in CC). Conclusions:We conclude that xenon, in the infant mouse brain, has paradoxical properties. It triggers neuroapoptosis, and when combined with isoflurane, it increases the depth of anesthesia, and retains its own apoptogenic activity. However, it suppresses, rather than augments, isoflurane's apoptogenic activity. CAN J ANESTH 2008 / 55: 7 / pp 429-436Objectif : Les médicaments supprimant l'activité neuronale, y compris tous les anesthésiants généraux testés jusqu 'à présent (kétamine, midazolam, isoflurane, propofol, et un cocktail de midazolam, de protoxyde d'azote et d'isoflurane)

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“…[2][3][4] Xenon, a rediscovered inhaled anesthetic with an extremely low blood-gas solubility of 0.115 to 0.14 5 and a minimum alveolar concentration (MAC) of 63 to 71%, 6,7 has proven its clinical safety and efficacy in the past. 8 With its ecological and pharmacological qualities, xenon is an interesting alternative to other inhaled anesthetics. The combination of a short-acting opioid, a short duration neuromuscular blocking drug such as mivacurium, and xenon may be of interest for fast-track anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Xenon does not modify mivacurium induced neuromuscular block

Kunitz

Baumert

Hecker

et al. 2005

Can J Anesth/J Can Anesth

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Purpose:The interaction between mivacurium and inhaled anesthetics is known, with the exception of xenon. We compared the pharmacodynamics of mivacurium during xenon anesthesia vs total iv anesthesia with propofol.Methods: This randomized controlled trial was carried out in the Aachen University Hospital. Forty-two adult patients ASA I or II, aged 18 to 60 yr, were randomized to receive either xenon or propofol anesthesia. Anesthesia was induced with propofol and remifentanil in both groups (each n = 21). The xenon group received xenon via facemask until an end-expiratory concentration of 60% was reached for one minute. Meanwhile, the acceleromyograph was calibrated and a train-of-four stimulation of the adductor pollicis muscle was started. After stabilization of the signal for five minutes, a single bolus of 0.16 mg·kg -1 mivacurium was injected. Anesthesia was maintained with xenon and remifentanil or with propofol and remifentanil.Results: There were no significant differences between groups with respect to onset time (xenon 180 ± 64 vs propofol 195 ± 77 sec; P = 0.39), duration (xenon 16.18 ± 4.97 vs propofol 15.68 ± 6.17 min; P = 0.73), recovery index (xenon 5.63 ± 2.48 vs propofol 5.73 ± 2.12 min; P = 0.42) and clinical recovery (xenon 8.75 ± 2.57 vs propofol 9.28 ± 2.28 min; P = 0.22). Conclusion:We conclude that the neuromuscular blocking effects of mivacurium are similar when given during propofol vs xenon anesthesia. (xénon 180 ± 64 vs propofol 195 ± 77 s ; P = 0,39), à sa durée (xénon 16,18 ± 4,97 vs propofol 15,68 ± 6,17 min ; P = 0,73), à l'indice de récupération (xénon 5,63 ± 2,48 vs propofol 5,73 ± 2,12 min ; P = 0,42) et à la récupération clinique (xénon 8,75 ± 2,57 vs propofol 9,28 ± 2,28 min ; P = 0,22). Objectif : L'interaction entre le mivacurium et les anesthésiques Résultats : Il n'y a pas eu de différence intergroupe significative quant au délai d'installation du bloc Conclusion : Les effets neuromusculaires bloquants du mivacurium sont similaires pendant l'anesthésie au propofol ou au xénon.T HE combination of a short-acting opioid and neuromuscular blocking drug, such as remifentanil and mivacurium, allow rapid emergence and recovery from anesthesia. 1 On the other hand, it is well known that most inhaled anesthetics variably prolong and enhance the effects of nondepolarizing neuromuscular blocking drugs, compared to total iv anesthesia. 2-4 Xenon, a rediscovered inhaled anesthetic with an extremely low blood-gas solubility of 0.115 to 0.14 5 and a minimum alveolar concentration (MAC) of 63 to 71%, 6,7 has proven its clinical safety and efficacy in the past. 8 With its ecological and pharmacological qualities, xenon is an interesting alternative to other inhaled anesthetics. The combination of a short-acting opioid, a short duration

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Multicenter Randomized Comparison of the Efficacy and Safety of Xenon and Isoflurane in Patients Undergoing Elective Surgery

Cited by 189 publications

References 15 publications

Cooling Combined with Immediate or Delayed Xenon Inhalation Provides Equivalent Long-Term Neuroprotection after Neonatal Hypoxia—Ischemia

Cooling Combined with Immediate or Delayed Xenon Inhalation Provides Equivalent Long-Term Neuroprotection after Neonatal Hypoxia—Ischemia

Potential of xenon to induce or to protect against neuroapoptosis in the developing mouse brain

Xenon does not modify mivacurium induced neuromuscular block

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