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[氯胺酮与诱发电位]

[Ketamine and evoked potentials].

作者信息

Kochs E, Bischoff P

机构信息

Institut für Anaesthesiologie, Klinikum rechts der Isar der Technischen Universität München.

出版信息

Anaesthesist. 1994 Nov;43 Suppl 2:S8-14.

PMID:7840419
Abstract

Ketamine-induced changes in the spontaneous and evoked electroencephalogram have been well documented in animals and humans. In contrast to the action of hypnotics, ketamine does not result in a dose-dependent suppression of neural activity. Many studies have revealed excitatory activity with induction of synchronized high-voltage slow waves in the electroencephalogram (EEG). Somatosensory evoked responses (SEP) have been found to be enhanced following induction of anaesthesia with ketamine. However, increases in amplitude were small compared with the SEP-enhancing effects of etomidate. The increase in somatosensory evoked responses may reflect dose-dependent disinhibition and/or increased excitation of cerebral neuronal activity induced by ketamine. Attenuation of late cortical somatosensory evoked responses following stimulation of thin C- and A delta-nerve fibres has been reported in volunteers given low-dose ketamine. Changes in SEP amplitude correlated to changes in subjective pain sensation. From this it was concluded that the analgesic effect of ketamine can be assessed by electrophysiological measurement methods. Recent studies suggest that the analgesic effect of the racematic ketamine mixture can probably be related to the effects of S-(+)-ketamine isomer, which has been shown to be involved in the activation of an opioidergic mechanism. Auditory evoked responses (AEP) of short latencies with origins in the brain stem have been shown to be slightly altered by ketamine. From this it was concluded that these components may not be used for assessment of the depth of anaesthesia. In contrast to the effects of hypnotics, mid-latency AEP components may be recorded during ketamine anaesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

氯胺酮引起的自发和诱发脑电图变化在动物和人类中已有充分记录。与催眠药的作用不同,氯胺酮不会导致神经活动的剂量依赖性抑制。许多研究揭示了脑电图(EEG)中同步高压慢波诱导的兴奋活动。发现氯胺酮麻醉诱导后体感诱发电位(SEP)增强。然而,与依托咪酯的SEP增强作用相比,幅度增加较小。体感诱发电位的增加可能反映了氯胺酮诱导的剂量依赖性去抑制和/或大脑神经元活动的兴奋增加。在给予低剂量氯胺酮的志愿者中,已报道刺激细C纤维和Aδ纤维后晚期皮质体感诱发电位减弱。SEP幅度的变化与主观疼痛感觉的变化相关。由此得出结论,氯胺酮的镇痛作用可以通过电生理测量方法进行评估。最近的研究表明,消旋氯胺酮混合物的镇痛作用可能与S-(+)-氯胺酮异构体的作用有关,该异构体已被证明参与阿片样物质机制的激活。起源于脑干的短潜伏期听觉诱发电位(AEP)已被证明会被氯胺酮轻微改变。由此得出结论,这些成分可能不能用于评估麻醉深度。与催眠药的作用不同,在氯胺酮麻醉期间可以记录中潜伏期AEP成分。(摘要截断于250字)

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