磷脂酶C相关的无活性1型蛋白缺乏影响小鼠行丙泊酚和依托咪酯麻醉诱导时脑电图活动
本公众号每天分享一篇最新一期Anesthesia & Analgesia等SCI杂志的摘要翻译，敬请关注并提出宝贵意见
Phospholipase C-related inactive protein type-1 deficiencyaffects anesthetic electroencephalogram activity induced by propofol and etomidate in mice
背景与目的
丙泊酚和依托咪酯主要通过GABAA受体(GABAA-R)发挥麻醉作用。GABAA-R活性是由磷脂酶c相关的非活性1型(PRIP-1)蛋白决定的，该蛋白与GABAA-R的亚细胞定位有关。PRIP-1的高效能减弱丙泊酚的行为反应，而不是依托咪酯。然而，这些麻醉剂和PRIP-1对中枢神经系统脑活动的影响仍不清楚。本研究我们观察了丙泊酚和依托咪酯对脑电图(EEG)的影响。
方 法
记录原生型(WT)和PRIP-1敲除(PRIP-1 KO)小鼠皮层脑电图(EEG)活动。对所有记录的脑电图数据进行精细分析，比较注射麻醉药前后脑电图信号的功率谱密度和95%的谱边频率。
结 果
PRIP-1缺陷导致EEG绝对功率增加，但在没有麻醉的情况下在醒来和睡眠状态期间频谱功率没有显着改变。异丙酚诱导WT小鼠低频脑电图活动相对增加，SEF95值降低，但对PRIP-1 KO小鼠无明显影响。注射依托咪酯后，两种基因型组的低频脑电图功率均有提高。在高频率下，PRIP-1 KO小鼠的相对功率小于WT小鼠。
结 论
缺乏PRIP-1能够干扰脑电图功率分布，但不影响依托咪酯给药后麻醉深度。我们的分析表明，PRIP-1通过调节GABAA-R活性，在麻醉脑电图活动中有不同程度的参与。
原始文献摘要
Furukawa T, Nikaido Y, Shimoyama S, Ogata Y, Kush. Phospholipase C-related inactive protein type-1 deficiencyaffects anesthetic electroencephalogram activity induced by propofol and etomidate in mice. J Anesth. 2019 Jul 22. doi: 10.1007/s00540-019-02663-z. [Epubahead of print] PubMed PMID: 31332527.
Purpose The general anesthetics propofol and etomidate mainly exert their anesthetic actions via GABA A receptor (GABAA-R). The GABAA-R activity is infuenced by phospholipase C-related inactive protein type-1 (PRIP-1), which is related to trafcking and subcellular localization of GABAA-R. PRIP-1 defciency attenuates the behavioral reactions to propofol but not etomidate. However, the efect of these anesthetics and of PRIP-1 defciency on brain activity of CNS are still unclear. In this study, we examined the efects of propofol and etomidate on the electroencephalogram (EEG).
Methods The cortical EEG activity was recorded in wild-type (WT) and PRIP-1 knockout (PRIP-1 KO) mice. All recorded EEG data were ofine analyzed, and the power spectral density and 95% spectral edge frequency of EEG signals were compared between genotypes before and after injections of anesthetics.
Results PRIP-1 defciency induced increases in EEG absolute powers, but did not markedly change the relative spectral powers during waking and sleep states in the absence of anesthesia. Propofol administration induced increases in low-frequency relative EEG activity and decreases in SEF95 values in WT but not in PRIP-1 KO mice. Following etomidate injection, low-frequency EEG power was increased in both genotype groups. At high frequency, the relative power in PRIP-1 KO mice was smaller than that in WT mice.
Conclusions The lack of PRIP-1 disrupted the EEG power distribution, but did not afect the depth of anesthesia after etomidate administration. Our analyses suggest that PRIP-1 is diferentially involved in anesthetic EEG activity with the
regulation of GABAA-R activity.
麻醉学文献进展分享
贵州医科大学高鸿教授课题组
翻译：代东君 编辑：何幼芹 审校：王贵龙