硫喷妥钠作用于神经活动的能量方面

Y. Mednikova, M. K. Kozlov, A. Makarenko
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引用次数: 3

摘要

以麻醉剂量使用的硫喷妥钠,使识别意识背后的神经过程和确定其紊乱的原因成为可能。在研究皮质脑电活动、单个神经细胞的脉冲和前肢肌肉的肌电活动时,发现硫喷妥钠阻断了一些需要能量支持的神经元反应:对神经元施加乙酰胆碱的强直激活反应停止;神经元自发活动率下降;皮肤电刺激反应的非特异性激活阶段消失。因此,硫喷妥钠通过显著限制大脑能量代谢来阻断意识。这导致了中枢神经系统适应性功能的丧失。同时,不依赖于能量支持形成的谷氨酸能兴奋对硫喷妥钠的作用有抗性。硫喷妥钠对大脑能量供应的阻断,根据其作用深度的不同,可分为缺氧和麻醉两个阶段。缺氧期伴有神经系统亢进,表现为脑电图上的癫痫样放电和强烈的无动机运动;麻醉阶段与运动活动阻滞和脑电图振荡趋平有关。与硫喷妥钠的缺氧作用有关的麻醉后状态导致离子稳态的丧失,并伴有皮层神经元峰值振幅的稳定下降。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Energy Aspects of Sodium Thiopental Action on Nervous Activity
Sodium thiopental, used in a narcotic dose, makes it possible to identify the nervous processes that underlie consciousness and establish the causes of its disorder. When studying the cortical EEG activity, the impulses of individual nerve cells and the electromyographic activity of the muscles of the forelimb, it was found that thiopental blocks a number of neuronal reactions requiring energy support: tonic activating reactions to acetylcholine, applied to neurons, cease; the rate of spontaneous neuronal activity drops; the stage of non-specific activation in response to electrocutaneous stimulation disappears. So, thiopental blocks consciousness by significant limitation of the brain energy metabolism. This results in a loss of the adaptive function of the central nervous system. At the same time, glutamatergic excitation, the formation of which does not depend on energy support, is resistant to the action of thiopental. The blocking of the brain’s energy supply caused by thiopental, in accordance with its depth, develops in two stages—hypoxic and narcotic. The hypoxic stage is accompanied by hyperactivity in the nervous system, which is manifested by epileptiform discharges on the EEG and powerful unmotivated movement; the narcotic stage is associated with blockade of motor activity and flattening of EEG oscillations. The post-narcotic state associated with the consequence of the hypoxic effect of thiopental leads to the loss of ionic homeostasis and is accompanied by a steady drop in the amplitude of cortical neuron spikes.
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