Akeju Oluwaseun, Hamilos Allison E, Song Andrew H, Pavone Kara J, Purdon Patrick L, Brown Emery N
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Harvard Medical School, Boston, MA, USA; Harvard-Massachusetts Institute of Technology Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA, USA; Institute for Medical Engineering and Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
Clin Neurophysiol. 2016 Jun;127(6):2472-81. doi: 10.1016/j.clinph.2016.02.012. Epub 2016 Feb 27.
An emerging paradigm for understanding how anesthetics induce altered arousal is relating receptor targeting in specific neural circuits to electroencephalogram (EEG) activity. Enhanced gamma amino-butyric acid A (GABAA) inhibitory post-synaptic currents (IPSCs) manifest with large-amplitude slow (0.1-1Hz) and frontally coherent alpha (8-12Hz) EEG oscillations during general anesthesia. Therefore, we investigated the EEG signatures of modern day derivatives of ether (MDDE) anesthesia to assess the extent to which we could obtain insights into MDDE anesthetic mechanisms.
We retrospectively studied cases from our database in which patients received isoflurane anesthesia vs. isoflurane/ketamine anesthesia (n=10 each) or desflurane anesthesia vs. desflurane/ketamine anesthesia (n=9 each). We analyzed the EEG recordings with spectral power and coherence methods.
Similar to known GABAA circuit level mechanisms, we found that MDDE anesthesia induced large amplitude slow and frontally coherent alpha oscillations. Additionally, MDDE anesthesia also induced frontally coherent theta (4-8Hz) oscillations. Reduction of GABAergic IPSCs with ketamine resulted in beta/gamma (13-40Hz) oscillations, and significantly reduced MDDE anesthesia-induced slow, theta and alpha oscillation power.
Large amplitude slow oscillations and coherent alpha and theta oscillations are moderated by ketamine during MDDE anesthesia.
These observations are consistent with the notion that GABAA circuit-level mechanisms are associated with MDDE anesthesia-induced unconsciousness.
一种用于理解麻醉剂如何诱导唤醒改变的新兴范式是将特定神经回路中的受体靶向与脑电图(EEG)活动联系起来。在全身麻醉期间,增强的γ-氨基丁酸A(GABAA)抑制性突触后电流(IPSCs)表现为大振幅慢波(0.1 - 1Hz)以及额叶相干α波(8 - 12Hz)脑电振荡。因此,我们研究了醚类现代衍生物(MDDE)麻醉的脑电图特征,以评估我们能在多大程度上深入了解MDDE的麻醉机制。
我们回顾性研究了数据库中的病例,其中患者接受异氟烷麻醉与异氟烷/氯胺酮麻醉(各10例)或地氟烷麻醉与地氟烷/氯胺酮麻醉(各9例)。我们用频谱功率和相干方法分析脑电图记录。
与已知的GABAA回路水平机制相似,我们发现MDDE麻醉诱导出大振幅慢波和额叶相干α波振荡。此外,MDDE麻醉还诱导出额叶相干θ波(4 - 8Hz)振荡。氯胺酮降低GABA能IPSCs导致β/γ波(13 - 40Hz)振荡,并显著降低MDDE麻醉诱导的慢波、θ波和α波振荡功率。
在MDDE麻醉期间,氯胺酮可调节大振幅慢波振荡以及相干α波和θ波振荡。
这些观察结果与GABAA回路水平机制与MDDE麻醉诱导的无意识状态相关这一观点一致。