Xenon Anesthesia

Lynch, Carl; Baum, J.; Tenbrinck, R.; Weiskopf, Richard B.

doi:10.1097/00000542-200003000-00031

Cited by 125 publications

(73 citation statements)

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“…Therefore, the replacement of N 2 O with Xe may become appropriate when delivery systems (i.e., closed circuit) become available with efficient techniques for recycling the gas to decrease the cost of Xe anesthesia. 30 In conclusion, 50% Xe produced cardiac effects identical to those of N 2 O or N 2 in isolated rat hearts under conditions of decreased O 2 delivery. Xe itself lacks cardiodepressant effects and may become a useful alternative to N 2 O.…”

Section: 516mentioning

confidence: 77%

Xenon and nitrous oxide do not depress cardiac function in an isolated rat heart model

Nakayama¹,

Takahashi

Okubo

et al. 2002

Can J Anesth/J Can Anesth

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Section: 516mentioning

confidence: 77%

Xenon and nitrous oxide do not depress cardiac function in an isolated rat heart model

Nakayama¹,

Takahashi

Okubo

et al. 2002

Can J Anesth/J Can Anesth

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“…A wide range of anaesthetic agents are now available and can be used especially in bigger animals like pigs and dogs as well as in humans. Xenon as an anaesthetic may prove to be superior to other anaesthetic agents (Lane et al 1980, Lynch et al 2000. It is of special interest to the physiologist because it is highly cardiostable.…”

Section: Discussionmentioning

confidence: 99%

The haemodynamic and catecholamine response to xenon/remifentanil anaesthesia in Beagle dogs

et al. 2008

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SummaryThe noble gas xenon seems to have minimal cardiovascular side-effects and so may be an ideal anaesthetic agent when investigating cardiovascular physiology. In comparison with standard modern anaesthetics, we investigated the haemodynamic and hormonal effects of xenon in Beagle dogs. After a 30 min baseline period, anaesthesia was induced with propofol and maintained with either (1) 1.2% isoflurane/70% nitrous oxide (N 2 O), (2) 0.8% isoflurane/ 0.5 mg/kg/min remifentanil or (3) 63% xenon/0.5 mg/kg/min remifentanil (n ¼ 6 per group).Haemodynamics were recorded and blood samples taken before and 60 min after induction. Mean arterial blood pressure (MAP) was higher in conscious dogs than during isoflurane/N 2 O (86 + 2 vs. 65 + 2 mmHg, mean + SEM) and isoflurane/remifentanil anaesthesia (95 + 2 vs. 67 + 3 mmHg), whereas MAP did not decrease significantly in response to xenon/ remifentanil anaesthesia (96 + 4 vs. 85 + 6 mmHg). Bradycardia was present during isoflurane/remifentanil (54 + 2/min) and xenon/remifentanil (40 + 3/min), but not during isoflurane/N 2 O anaesthesia (98 + 3/min, P , 0.05). Xenon/remifentanil anaesthesia induced the highest reduction in cardiac output (CO) ( -61%), and the highest increase in systemic vascular resistance (þ120%) among all treatment groups (P , 0.05). A simultaneous increase in endogenous adrenaline and noradrenaline concentrations could only be observed in the xenon/remifentanil group, whereas angiotensin II and vasopressin concentrations increased in all groups. In conclusion, xenon/remifentanil anaesthesia maintains MAP but reduces heart rate and CO and is associated with a considerable stimulation of vasopressor hormones in Beagle dogs. Therefore, xenon/remifentanil exerts a new quality of adverse haemodynamic effects different from volatile anaesthetics and may not perform better during studies of cardiovascular physiology.

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“…For comparison, another cohort of pups (n ¼ 5) were exposed to 70% nitrous oxide (N 2 O) balanced with oxygen for 120 mins. This gas has a similar anaesthetic potency in this species (Lynch et al, 2000;Russel and Graybeal, 1992). Four hours later, the pups underwent right common carotid artery ligation followed by hypoxia.…”

Section: In Vivo Hypoxia-ischaemiamentioning

confidence: 99%

Xenon Preconditioning Reduces Brain Damage from Neonatal Asphyxia in Rats

Hossain

Pettet

et al. 2006

J Cereb Blood Flow Metab

166

111

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Xenon attenuates on-going neuronal injury in both in vitro and in vivo models of hypoxic-ischaemic injury when administered during and after the insult. In the present study, we sought to investigate whether the neuroprotective efficacy of xenon can be observed when administered before an insult, referred to as 'preconditioning'. In a neuronal-glial cell coculture, preexposure to xenon for 2 h caused a concentration-dependent reduction of lactate dehydrogenase release from cells deprived of oxygen and glucose 24 h later; xenon's preconditioning effect was abolished by cycloheximide, a protein synthesis inhibitor. Preconditioning with xenon decreased propidium iodide staining in a hippocampal slice culture model subjected to oxygen and glucose deprivation. In an in vivo model of neonatal asphyxia involving hypoxic-ischaemic injury to 7-day-old rats, preconditioning with xenon reduced infarction size when assessed 7 days after injury. Furthermore, a sustained improvement in neurologic function was also evident 30 days after injury. Phosphorylated cAMP (cyclic adenosine 3 0 ,5 0 -monophosphate)-response element binding protein (pCREB) was increased by xenon exposure. Also, the prosurvival proteins Bcl-2 and brain-derived neurotrophic factor were upregulated by xenon treatment. These studies provide evidence for xenon's preconditioning effect, which might be caused by a pCREB-regulated synthesis of proteins that promote survival against neuronal injury.

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Xenon Anesthesia

Cited by 125 publications

References 0 publications

Xenon and nitrous oxide do not depress cardiac function in an isolated rat heart model

Xenon and nitrous oxide do not depress cardiac function in an isolated rat heart model

The haemodynamic and catecholamine response to xenon/remifentanil anaesthesia in Beagle dogs

Xenon Preconditioning Reduces Brain Damage from Neonatal Asphyxia in Rats

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