Nishiyama Y
Department of Anesthesia, Ehime Rousai Hospital, Niihama.
Masui. 1990 Aug;39(8):984-7.
The effects of ketamine with 60% nitrous oxide were studied on subcortical sensory evoked potentials recorded at Erb's point (N9), neck (N13) and on cortical potentials recorded at the scalp (N20) following median nerve stimulations in 7 neurologically normal patients. Latencies and amplitudes of the potentials were measured and compared with postinduction control values taken during inhalation of 60% nitrous oxide. Ketamine 2 mg.kg-1 (iv) was administered initially and incremental dose was 50 micrograms.kg-1.min-1. N20 latency decreased at 15, 30 minutes after ketamine administration from a control value of 18.7 +/- 0.9 msec to 18.2 +/- 1.1, 18.2 +/- 1.1 msec respectively, and N13-N20 interpeak latency decreased from 6.0 +/- 0.4 msec to 5.5 +/- 0.7, 5.4 +/- 0.7 msec (mean +/- SD). The author concluded that during nitrous oxide-based anesthesia, ketamine did not inhibit specific thalamoneocortical pathways.
在7例神经功能正常的患者中，研究了氯胺酮与60%氧化亚氮联合应用对正中神经刺激后在Erb点（N9）、颈部（N13）记录的皮层下感觉诱发电位以及头皮记录的皮层电位（N20）的影响。测量了电位的潜伏期和波幅，并与吸入60%氧化亚氮期间的诱导后对照值进行比较。初始静脉注射氯胺酮2mg·kg-1，增量剂量为50μg·kg-1·min-1。氯胺酮给药后15、30分钟时，N20潜伏期从对照值18.7±0.9毫秒分别降至18.2±1.1、18.2±1.1毫秒，N13-N20峰间潜伏期从6.0±0.4毫秒降至5.5±0.7、5.4±0.7毫秒（均数±标准差）。作者得出结论，在基于氧化亚氮的麻醉期间，氯胺酮并未抑制特定的丘脑皮质通路。
