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麻醉诱导昏迷大脑的超敏反应。

Hypersensitivity of the anesthesia-induced comatose brain.

作者信息

Kroeger Daniel, Amzica Florin

机构信息

Laboratoire de Neurophysiologie, Centre de Recherche Université Laval Robert-Giffard, Quebec, Quebec, Canada G1J 2G3.

出版信息

J Neurosci. 2007 Sep 26;27(39):10597-607. doi: 10.1523/JNEUROSCI.3440-07.2007.

Abstract

Increasing levels of anesthesia are thought to produce a progressive loss of brain responsiveness to external stimuli. Here, we present the first report of a state window within anesthesia-induced coma, usually associated with an EEG pattern of burst suppression, during which brain excitability is dramatically increased so that even subliminal stimuli elicit bursts of whole-brain activity. We investigated this phenomenon in vivo using intracellular recordings of both neurons and glia, as well as extracellular calcium and EEG recordings. The results indicate that the bursting activity elicited with mechanical microstimulations, but also with auditory and visual stimuli, is dependent on complex mechanisms, including modulation of excitatory (NMDA) components, gap junction transmission, as well as the extracellular calcium concentration. The occurrence of bursting events is associated with a postburst refractory period that underlies the genesis of the alternating burst-suppression pattern. These findings raise the issue of what burst spontaneity during anesthesia-induced coma means and opens new venues for the handling of comatose patients.

摘要

麻醉深度增加被认为会使大脑对外界刺激的反应性逐渐丧失。在此,我们首次报告了麻醉诱导昏迷期间存在一个状态窗口,通常与爆发抑制脑电图模式相关,在此期间大脑兴奋性显著增加,以至于即使是阈下刺激也能引发全脑活动的爆发。我们使用神经元和神经胶质细胞的细胞内记录以及细胞外钙和脑电图记录在体内研究了这一现象。结果表明,机械微刺激以及听觉和视觉刺激引发的爆发活动依赖于复杂的机制,包括兴奋性(NMDA)成分的调节、缝隙连接传递以及细胞外钙浓度。爆发事件的发生与爆发后不应期相关,后者是交替爆发抑制模式产生的基础。这些发现提出了麻醉诱导昏迷期间爆发自发性意味着什么的问题,并为昏迷患者的治疗开辟了新途径。

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