Antognini J F, Carstens E, Sudo M, Sudo S
Department of Anesthesiology and Pain Medicine, Section of Neurobiology, Physiology and Behavior, University of California, Davis, California 95616, USA.
Anesth Analg. 2000 Nov;91(5):1282-8.
Anesthetics such as isoflurane act in the spinal cord to suppress movement in response to noxious stimulation. Spinal anesthesia decreases hypnotic/sedative requirements, possibly by decreasing afferent transmission of stimuli. We hypothesized that isoflurane action in the spinal cord would similarly depress the ascending transmission of noxious input to the thalamus and cerebral cortex. In six isoflurane-anesthetized goats, we measured electroencephalographic (EEG) and thalamic single-unit responses to a clamp applied to the forelimb. Cranial bypass permitted differential isoflurane delivery to the torso and cranial circulations. When the cranial-torso isoflurane combination was 1.3% +/- 0.2%-1.0% +/- 0.4% the noxious stimulus did not evoke significant changes in the EEG or thalamic activity: 389 (153-544) to 581 (172-726) impulses/min, (median, 25th-75th percentile range, P: > 0.05). When the cranial-torso isoflurane combination was 1.3% +/- 0.2%-0.3% +/- 0.2%, noxious stimulation increased thalamic activity: 804 (366-1162) to 1124 (766-1865) impulses/min (P: < 0.05), and the EEG "desynchronized": total EEG power decreased from 25 +/- 20 microV(2) to 12 +/- 8 microV(2) (P: < 0.05). When the cranial-torso isoflurane was 1.7% +/- 0.1%-0.3% +/- 0.2%, the noxious stimulus did not significantly affect thalamic: 576 (187-738) to 1031 (340-1442) impulses/min (P: > 0.05), or EEG activity. The indirect torso effect of isoflurane on evoked EEG total power (12.6 +/- 2.7 microV(2)/vol%, mean +/- SE) was quantitatively similar to the direct cranial effect (17.7 +/- 3.0 microV(2)/vol%; P: > 0.05). These data suggest that isoflurane acts in the spinal cord to blunt the transmission of noxious inputs to the thalamus and cerebral cortex, and thus might indirectly contribute to anesthetic endpoints such as amnesia and unconsciousness.
Isoflurane action in the spinal cord diminished the transmission of noxious input to the brain. Because memory and consciousness are likely dependent on the "arousal" state of the brain, this indirect action of isoflurane could contribute to anesthetic-induced amnesia and unconsciousness.
异氟烷等麻醉剂在脊髓中起作用，以抑制对有害刺激的运动反应。脊髓麻醉可能通过减少刺激的传入传递来降低催眠/镇静需求。我们假设异氟烷在脊髓中的作用会类似地抑制有害输入向丘脑和大脑皮层的上行传递。在六只接受异氟烷麻醉的山羊中，我们测量了脑电图（EEG）和丘脑对施加在前肢上的夹子的单单位反应。颅外分流允许将异氟烷分别输送到躯干和颅循环。当颅-躯干异氟烷组合为1.3%±0.2%-1.0%±0.4%时，有害刺激未引起脑电图或丘脑活动的显著变化：从389（153 - 544）次/分钟到581（172 - 726）次/分钟，（中位数，第25 - 75百分位数范围，P：>0.05）。当颅-躯干异氟烷组合为1.3%±0.2%-0.3%±0.2%时，有害刺激增加了丘脑活动：从804（366 - 1162）次/分钟到1124（766 - 1865）次/分钟（P：<0.05），并且脑电图“去同步化”：脑电图总功率从25±20微伏²降至12±8微伏²（P：<0.05）。当颅-躯干异氟烷为1.7%±0.1%-0.3%±0.2%时，有害刺激对丘脑没有显著影响：从576（187 - 738）次/分钟到1031（340 - 1442）次/分钟（P：>0.05），对脑电图活动也无显著影响。异氟烷对诱发脑电图总功率的间接躯干效应（12.6±2.7微伏²/体积%，平均值±标准误差）在数量上与直接颅效应（17.7±3.0微伏²/体积%；P：>0.05）相似。这些数据表明，异氟烷在脊髓中起作用，以减弱有害输入向丘脑和大脑皮层的传递，因此可能间接促成诸如失忆和无意识等麻醉终点。
异氟烷在脊髓中的作用减少了有害输入向大脑的传递。由于记忆和意识可能依赖于大脑的“唤醒”状态，异氟烷的这种间接作用可能促成麻醉诱导的失忆和无意识。
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