Xenon anaesthesia is associated with a reduction in frontal electroencephalogram peak alpha frequency

Steven McGuigan , Andria Pelentritou , David A. Scott , Jamie Sleigh
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Abstract

Background

Administration of conventional anaesthetic agents is associated with changes in electroencephalogram (EEG) oscillatory dynamics, including a reduction in the peak alpha frequency. Computational models of neurones can reproduce such phenomena and are valuable tools for investigating their underlying mechanisms. We hypothesised that EEG data acquired during xenon anaesthesia in humans would show similar changes in peak alpha frequency and that computational neuronal models of recognised cellular actions of xenon would be consistent with the observed changes.

Methods

EEG recordings were obtained for 11 participants from a randomised controlled trial of xenon anaesthesia and for 21 participants from a volunteer study of xenon administration. The frontal peak alpha frequency was calculated for both cohorts at awake baseline and during xenon administration. In silico simulations with two computational models of neurones were performed to investigate how xenon antagonism of hyperpolarisation-activated cyclic nucleotide-gated channel 2 (HCN2) and glutamatergic excitatory neurotransmission would influence peak alpha frequency.

Results

Compared with awake baseline, frontal peak alpha frequency was significantly lower during xenon administration in the randomised controlled trial cohort, median (inter-quartile range) frequency 7.73 Hz (7.27–8.08 Hz) vs 8.81 Hz (8.35–9.03 Hz), P=0.012, and the volunteer cohort, 8.69 Hz (8.34–8.98 Hz) vs 9.41 Hz (9.11–9.92 Hz), P=0.001. In silico simulations with both computational models suggest that antagonism of HCN2 and glutamatergic excitatory neurotransmission are associated with a reduction in peak alpha frequency.

Conclusions

Xenon administration is associated with a reduction of peak alpha frequency in the frontal EEG. In silico simulations utilising two computational models of neurones suggest that these changes are consistent with antagonism of HCN2 and glutamatergic excitatory neurotransmission.

Clinical trial registration

The Australian New Zealand Clinical Trials Registry: ANZCTR number 12618000916246.
氙气麻醉与额叶脑电图α峰频率降低有关
背景:常规麻醉药的施用与脑电图振荡动力学的变化有关,包括α峰频率的降低。神经元的计算模型可以再现这种现象,并且是研究其潜在机制的宝贵工具。我们假设人类在氙气麻醉期间获得的脑电图数据将显示出类似的α峰频率变化,并且识别氙气细胞作用的计算神经元模型将与观察到的变化一致。方法收集11例氙气麻醉随机对照试验和21例氙气给药志愿者的脑电图记录。计算两组受试者在清醒基线和氙气治疗期间的额叶α峰频率。利用两种神经元计算模型进行了计算机模拟,研究了超极化激活的环核苷酸门控通道2 (HCN2)和谷氨酸能兴奋性神经传递的氙拮抗作用如何影响α峰频率。结果与清醒基线相比,随机对照试验队列中(四分位数范围)中位频率7.73 Hz (7.27-8.08 Hz) vs 8.81 Hz (8.35-9.03 Hz)显著降低,志愿者队列中(四分位数范围)中位频率为8.69 Hz (8.34-8.98 Hz) vs 9.41 Hz (9.11-9.92 Hz), P=0.012。两种计算模型的计算机模拟表明,HCN2和谷氨酸能兴奋性神经传递的拮抗作用与α峰频率的降低有关。结论氙气处理与额叶脑电图α峰频率降低有关。利用两种神经元计算模型的计算机模拟表明,这些变化与HCN2和谷氨酸能兴奋性神经传递的拮抗作用是一致的。临床试验注册澳大利亚新西兰临床试验注册中心:ANZCTR编号12618000916246。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
BJA open
BJA open Anesthesiology and Pain Medicine
CiteScore
0.60
自引率
0.00%
发文量
0
审稿时长
83 days
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