Xenon: recent developments

Dingley, John; Ivanova-Stoilova, T. M.; Grundler, S.; Wall, T.

doi:10.1046/j.1365-2044.1999.00807.x

Cited by 69 publications

(28 citation statements)

References 64 publications

(94 reference statements)

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“…Minimal alveolar concentration (MAC) of Xe is 71% and that of N 2 O is 105% in humans. 2 In addition, the increase in norepinephrine release in the mPOA was more pronounced than in the PH. The mPOA is thought to be involved in the neuronal circuit eliciting the regulation of consciousness.…”

Section: Discussionmentioning

confidence: 91%

Xenon inhalation increases norepinephrine release from the anterior and posterior hypothalamus in rats

Yoshida

Kushikata

Kubota

et al. 2001

Can J Anesth/J Can Anesth

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Purpose: To investigate the effect of xenon (Xe) and nitrous oxide (N 2 O) on norepinephrinergic neuronal activity in the rat medial preoptic area (mPOA) and posterior hypothalamus (PH) using microdialysis.Methods: Sixty male Wistar rats were equally allocated to two groups: mPOA and PH. A microdialysis probe was implanted into the mPOA or the PH. In both groups, each animal was exposed to one of the following inhalations: 25% oxygen (control, n=6), 30% Xe (n=6), 60% Xe (n=6), 30% N 2 O (n=6) or 60% N 2 O (n=6). Norepinephrine concentration in the perfused artificial cerebrospinal fluid was measured by high pressure liquid chromatography at ten-minute intervals. After plotting the time-norepinephrine concentration curve, the area under the curve (AUC) in each group was calculated.Results: In the mPOA, 30 and 60% Xe, but only 60% N 2 O significantly increased norepinephrine release. The AUC in the 30% Xe, 60% Xe or 60% N 2 O group was 160 ± 9 (P <0.05), 288 ± 42 (P <0.01) or 237 ± 46 pg·min/sample (P <0.01), respectively, compared to that in the control group: 77 ± 14 pg·min/sample. In the PH, only 60% Xe significantly increased norepinephrine release compared to control (AUC: 191 ± 38 vs 71 ± 1 pg·min/sample, P <0.01).Conclusion: The present data suggest that Xe stimulates norepinephrinergic neurons more potently than N 2 O; 1.2 times more in the mPOA and 2.5 times more in the PH. This stimulant effect may contribute to the hypnotic and sympathotonic effects of Xe in rats.

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Section: Discussionmentioning

confidence: 91%

Xenon inhalation increases norepinephrine release from the anterior and posterior hypothalamus in rats

Yoshida

Kushikata

Kubota

et al. 2001

Can J Anesth/J Can Anesth

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“…The possibility of using xenon gas as an anaesthetic gas has also been suggested although its cost precludes its widespread use. 19 RESEARCH health and safety A recent report by the General Dental Council 20 highlighted that both conscious sedation and general anaesthesia must only be carried out in areas where suitable equipment and adequate facilities are available and only by an individual specifically trained to the requirements of the Royal College of Anaesthetists. Standards for General Anaesthesia in dentistry, published by the Royal College of Anaesthetists, questions the need for such a high proportion of procedures carried out under general anaesthesia in the UK 21 but the report fails to point out the importance of controlling exposure to anaesthetic agents in areas carrying out general anaesthesia.…”

Section: Discussionmentioning

confidence: 99%

Environmental monitoring of nitrous oxide during dental anaesthesia

Henderson

Matthews

2000

Br Dent J

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AimThe study was carried out to see if levels of nitrous oxide in dental theatres and community dental clinics were being controlled in accordance with the Control of Substances Hazardous to Health Regulations. Setting A multi-centre study looked at exposure levels in a dental teaching hospital and two community dental clinics in the South Wales area between 1997 and 1998. Methods A MIRAN infra-red spectrophotometer was used to measure static levels of nitrous oxide during general anaesthesia and conscious sedation. NIOSH method 6600 was used to collect personal samples of the individual administering the anaesthetic. Results The results showed compliance with the regulations when averaged out over an 8 hour time weighted average. However, over short periods of time peak concentrations of up to 1190 ppm were observed through static sampling, and up to 734 ppm through personal sampling. Conclusions The results highlighted the need to provide adequate control measures such as anaesthetic gas scavenging, to reduce occupational exposure to dental staff in dental operating theatres and community dental clinics, therefore providing a safe working environment.

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“…42 Although xenon is expensive, cost-efficient methods of delivery are being developed. 13 There is a need for effective neuroprotective strategies in many areas of medicine, and we suggest that neonatology should be a high priority, given the current limited effective alternatives and the profound impact of neonatal brain damage on the future life of the affected baby and the consequent financial impact on society.…”

Section: Dingley Et Al Xenon Neuroprotection 503mentioning

confidence: 99%

“…It is an effective anesthetic with a very rapid onset, no metabolism by the body, and no proven adverse hemodynamic clinical side effects, unlike many other inhaled agents. [12][13][14][15] However, xenon is expensive, which has limited its clinical use. Xenon has been shown recently to be neuroprotective in vitro and in vivo in rats when administered during hypoxia.…”

mentioning

confidence: 99%

Xenon Provides Short-Term Neuroprotection in Neonatal Rats When Administered After Hypoxia-Ischemia

Dingley

Tooley

Porter

et al. 2006

Stroke

179

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Background and Purpose-Brain injury after hypoxic-ischemic insults evolves via an apoptotic/necrotic cascade.Glutamate over release and N-methyl-D-aspartate (NMDA) receptor over activation (excitotoxicity) are believed to trigger this process. Xenon is a nontoxic anesthetic gas that reduces neurotransmitter release and functionally antagonizes NMDA receptors. Administering xenon to hypoxic-ischemic newborns might be clinically effective if the neurotoxic processes continue evolving after delivery. We sought to determine whether xenon administration after the initial hypoxic-ischemic insult was neuroprotective. Methods-Fifty 7-day-old rats received a 90-minute hypoxic insult after unilateral carotid ligation. They were then randomized to breathe 1 of 2 gas mixtures for 3 hours: 50% Xe/30% O 2 /20% N 2 or 30% O 2 /70% N 2 . Results-One week after hypoxic-ischemic survival, significant global protection was seen in the xenon group (80% less injury); cortex/white matter (88% versus 25%), hippocampus (62% versus 0%), basal ganglia (81% versus 25%), and thalamus (50% versus 0%; percentage of global damage score in nonxenon versus xenon groups, respectively). Conclusions-Three hours of xenon administration commenced after hypoxia-ischemia in neonatal rats provides short-term neuroprotection. This finding suggests that treatment with xenon after perinatal asphyxia would also be neuroprotective. Because xenon does not cause other neurotoxic effects and has demonstrated minimal side effects in extensive anesthesia studies, it would make an ideal candidate for the treatment after human perinatal hypoxia-ischemia.

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Xenon: recent developments

Cited by 69 publications

References 64 publications

Xenon inhalation increases norepinephrine release from the anterior and posterior hypothalamus in rats

Xenon inhalation increases norepinephrine release from the anterior and posterior hypothalamus in rats

Environmental monitoring of nitrous oxide during dental anaesthesia

Xenon Provides Short-Term Neuroprotection in Neonatal Rats When Administered After Hypoxia-Ischemia

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