Deeprose C, Andrade J, Harrison D, Edwards N
Department of Psychology, University of Sheffield, Western Bank, Sheffield, S10 2TP, UK.
Br J Anaesth. 2005 Jan;94(1):57-62. doi: 10.1093/bja/aeh289. Epub 2004 Oct 14.
Priming during anaesthesia has been hard to replicate and the conditions under which it occurs remain poorly understood. We replicated and extended a recent study to determine whether intraoperative priming during propofol and nitrous oxide anaesthesia is a reliable phenomenon, whether it occurs due to awareness during word presentation and whether it is suppressed by a dose of fentanyl at induction.
Words were played through headphones during surgery to 62 patients receiving propofol and nitrous oxide anaesthesia. Thirty-two patients received fentanyl 1.5 microg kg(-1) at induction and 30 received no fentanyl. Neuromuscular blocking drugs were not used. Depth of anaesthesia was measured using the bispectral index (BIS). Anaesthetic variables were recorded at 1 min intervals during word presentation. On recovery, implicit and explicit memory were assessed using an auditory word-stem completion test and a yes-no word-recognition test, respectively.
BIS, blood pressure, end-tidal carbon dioxide and heart rate during word presentation did not differ between the study groups. The infusion rate of propofol and the patients' ventilatory frequency were significantly higher in the group not receiving fentanyl. No patient had unprompted explicit recall of surgery, although there was above-zero performance in six patients on the yes-no recognition task (P<0.05). There was no physiological evidence of awareness during anaesthesia (median mean-BIS=38 in the no-fentanyl group and 42 in the fentanyl group). There was evidence for priming (mean priming score=0.09, P<0.05 in the no-fentanyl study group; mean priming score=0.07, P<0.05 in the fentanyl group) even when patients with momentary light anaesthesia (maximum recorded BIS> or =60) and/or positive recognition scores were excluded from the analysis.
Existing knowledge can be primed by information presented during propofol and nitrous oxide anaesthesia. This priming is evidence of unconscious information processing and not the result of moments of awareness.
麻醉期间的启动效应很难复制，其发生的条件仍知之甚少。我们重复并扩展了一项近期研究，以确定丙泊酚和氧化亚氮麻醉期间的术中启动效应是否为可靠现象，其是否因单词呈现期间的知晓而发生，以及诱导时一剂芬太尼是否能抑制该效应。
手术期间通过耳机向62例接受丙泊酚和氧化亚氮麻醉的患者播放单词。32例患者在诱导时接受1.5微克/千克的芬太尼，30例未接受芬太尼。未使用神经肌肉阻滞药物。使用脑电双频指数（BIS）测量麻醉深度。在单词呈现期间每隔1分钟记录麻醉变量。恢复时，分别使用听觉单词词干补全测试和是非单词识别测试评估内隐记忆和外显记忆。
单词呈现期间，研究组之间的BIS、血压、呼气末二氧化碳和心率无差异。未接受芬太尼的组中丙泊酚输注速率和患者通气频率显著更高。尽管在是非识别任务中有6例患者表现高于零（P<0.05），但没有患者能主动明确回忆起手术过程。麻醉期间没有知晓的生理证据（未用芬太尼组中位平均BIS = 38，芬太尼组为42）。即使将短暂浅麻醉（记录的最大BIS≥60）和/或阳性识别分数的患者排除在分析之外，仍有启动效应的证据（未用芬太尼研究组平均启动分数 = 0.09，P<0.05；芬太尼组平均启动分数 = 0.07，P<0.05）。
丙泊酚和氧化亚氮麻醉期间呈现的信息可启动现有知识。这种启动效应是无意识信息处理的证据，而非知晓时刻的结果。
