Orth M, Barter L, Dominguez C, Atherley R, Carstens E, Antognini J F
Department of Anesthesiology and Pain Medicine, University of California, Davis, 95616, USA.
Br J Anaesth. 2005 Oct;95(4):477-84. doi: 10.1093/bja/aei208. Epub 2005 Jul 28.
Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up.
Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8x or 1.2x the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED(50)) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s).
Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from approximately 6 to approximately 8.5 Hz, and the SEF from approximately 25.5 to approximately 27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED(50) propofol, only the tail clamp and 1 Hz stimuli increased MEF ( approximately 8 to approximately 10-10.5 Hz). At the higher propofol infusion rate (1.2 ED(50)) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from approximately 23 to approximately 21.5 Hz).
Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.
麻醉药可减弱神经元对伤害性刺激的反应,包括对脑电图(EEG)反应的影响。目前尚不清楚不同麻醉药在调节伤害性刺激诱发的EEG激活方面的能力有何差异。我们研究了丙泊酚和氟烷对EEG对伤害性刺激反应的作用,包括重复性电C纤维刺激,这种刺激通常会诱发神经元累加效应。
将大鼠用氟烷(n = 8)或丙泊酚(n = 8)麻醉,剂量为引起对夹尾反应不动所需剂量的0.8倍或1.2倍[氟烷的最低肺泡浓度(MAC)和丙泊酚的半数有效剂量(ED50)]。我们记录了EEG对重复性电刺激序列(以0.1、1和3Hz施加于尾部)以及超强伤害性尾部刺激(夹尾;50Hz电刺激,每次持续30s)的反应。
在氟烷麻醉下,伤害性刺激诱发了EEG激活反应,表现为频谱边缘频率(SEF)和中位边缘频率(MEF)增加。在0.8MAC氟烷时,夹尾使MEF从约6Hz增加到约8.5Hz,SEF从约25.5Hz增加到约27Hz。在0.8和1.2MAC氟烷时,1Hz、3Hz和强直刺激序列观察到类似的EEG激活模式,但0.1Hz刺激未观察到,因为该刺激不会诱发累加效应。在丙泊酚麻醉下,伤害性刺激通常不会引起EEG激活。在0.8ED50丙泊酚时,只有夹尾和1Hz刺激使MEF增加(约8Hz至约10 - 10.5Hz)。在较高的丙泊酚输注速率(1.2ED50)下,重复性电刺激未诱发EEG反应,但强直刺激和夹尾反而使SEF降低(从约23Hz降至约21.5Hz)。
与氟烷相比,丙泊酚对EEG对伤害性刺激的反应具有更显著的减弱作用。