在麻醉致意识消失期间丙泊酚和乙托咪酯对大脑皮质、丘脑及网状结构神经元的抑制作用  

作　　者：Jason Andrada, MS Preetha Livingston, BS Bong Jae Lee, MD, PhD Joseph Antognini, MD, MBA 谢珺田(译) 宋文阁(校) 

机构地区：[1]Department of Anesthesiology and Pain Medicine, University of California, Davis, Davis, California [2]Department of Anesthesiology, Kyung Hee University Hospital at Gangdong, Seoul, Korea [3]不详

出　　处：《麻醉与镇痛》2013年第6期82-91,共10页Anesthesia & Analgesia

摘　　要：背景麻醉致意识消失的作用位点仍不清楚。可能的位点包括大脑皮质、丘脑和网状结构。我们研究了丙泊酚和乙托咪酯对正常动物皮质、丘脑及网状结构神经元功能的影响。方法对5只猫在麻醉状态下放置记录套管和脑电波螺丝钉电极。经过5天恢复期之后，每周重复检查3～4次。在给予丙泊酚或乙托咪酯注射之前、注射期间和注射之后记录大脑皮质（7、18和19区）、丘脑（腹后外侧核、腹后内侧核和内侧膝状体）及网状结构（中脑网状核群和中央被盖区）单个神经元的电活动。皮质神经元的动作电位按脉冲神经元和快速放电神经元分别进行分析。结果丙泊酚和乙托咪酯使皮质神经元自发放电频率降低37％-41％。两种麻醉剂对脉冲神经元和快速放电神经元的作用相似。丙泊酚和乙托咪酯亦使丘脑和网状结构神经元放电频率减低30％～49％。麻醉剂输注期间皮质、丘脑及网状结构脑电图表现相似，均从低幅高频快波变为高幅低频慢波；功率峰值发生于丙泊酚输注期间，频率为12～13Hz。乙托咪酯麻醉期间有2个大的峰值：一个频率为12—14Hz，另一个为7～8Hz。检测过程中猫处于深度镇静状态，瞬目反射和动须反射消失而伤害性刺激}】起的退缩反应保存。结论数据资料显示丙泊酚和乙托咪酯抑制大脑皮质、丘脑及网状结构神经元的作用相似。尽管麻醉剂对神经元电活动的抑制作用可能是麻醉剂致意识消失的潜在机制，但仍需进一步研究阐明上述位点的麻醉剂效应如何相互影响而终致意识消失。BACKGROUND： The sites where anesthetics produce unconsciousness are not well understood. Likely sites include the cerebral cortex, thalamus, and reticular formation. We examined the effects of propofol and etomidate on neuronal function in the cortex, thalamus, and reticular formation in intact animals. METHODS： Five cats had a recording well and electroencephalogram screws placed under anesthesia. After a 5-day recovery period, the cats were repeatedly studied 3 to 4 times per week. Neuronal （single-unit） activity in the cerebral cortex （areas 7, 18 and 19）, thalamus （ventral posterolateral and ventral posteromedial nuclei and medial geniculate body）, and reticular formation （mesencephalic reticular nucleus and central tegrnental field） was recorded before, during, and after infusion of either propofol or etomidate. Cortical neuronal action potentials were analyzed separately as either regular spiking neurons or fast spiking neurons. RESULTS： Propofol and etomidate decreased the spontaneous firing rate of cortical neurons by 37% to 41% ; fast spiking neurons and regular spiking neurons were similarly affected by the anesthetics. The neuronal firing rate in the thalamus and reticular formation decreased 30% to 49% by propofol and etomidate. The electroencephalogram shifted from a low-amplitude, high-frequency pattern to a high-amplitude, low-frequency pattern during drug infusion suggesting an anesthetic effect; peak power occurred at 12 to 13 Hz during propofol infusion. There were 2 maior peaks during etomidate anesthesia： one at 12 to 14 Hz and another at 7 to 8 Hz. The cats were heavily sedated, with depressed corneal and whisker reflexes; withdrawal to noxious stimulation remained intact. CONCLUSION： These data show that neurons in the cortex, thalamus, and reticular formation are similarly depressed by propofol and etomidate. Although anesthetic depression of neuronal activity likely contributes to anesthetic-induced unconsciousness, further work is needed to determine how anesthet

关 键 词：神经元功能 乙托咪酯 网状结构 大脑皮质 麻醉状态 抑制作用 丙泊酚 丘脑 

分 类 号：R778.11[医药卫生—眼科]