丙泊酚作用机制的功能性磁共振成像研究
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摘要
第一部分丙泊酚麻醉作用的脑电双频谱指数研究和功能性磁共振成像研究
目的
应用脑电双频谱指数监测(BIS)和血氧水平依赖的功能性磁共振成像(BOLD-fMRI),观察丙泊酚麻醉作用在人脑中枢的敏感部位。
方法
20名男性健康志愿者随机分为2组:浅麻醉组(BIS 60～80)和深麻醉组(BIS 40～60)。先行预试验,靶控输注丙泊酚。浅麻醉组,计算预试验中每个受试者BIS 80点和BIS 60点的丙泊酚效应室浓度(ESC)的平均数,以此作为该受试者的目标ESC。深麻醉组,计算BIS 60点和BIS 40点的丙泊酚ESC的平均数,以此作为目标ESC。预试验后1～2周内进行fMRI研究。扫描序列为:结构像+麻醉扫描(事件相关设计:时间15min=4min空白扫描+约9min输注丙泊酚扫描+约2min达目标ESC后扫描),深麻醉组还需进行苏醒扫描(事件相关设计:时间15min=4min目标丙泊酚ESC扫描+11min停止输注后扫描)。记录扫描期间监护仪数值,以及扫描前后观察者觉醒/镇静评分(OAA/S)评分。使用SPM2、Matlab 6.5软件进行fMRI图像分析。
结果
①浅麻醉组(BIS 60～80,OAA/S 3分)丙泊酚麻醉所激活的脑区,仅有左顶下小叶区。②深麻醉组(BIS 40～60,OAA/S 1分)丙泊酚麻醉所激活的脑区,为左岛叶,左颞上回,右颞中回。③浅麻醉—深麻醉所激活的脑区较多,两侧岛叶、颞叶、边缘叶和左基底核、中脑均有脑区激活。④深麻醉—浅麻醉、苏醒期、深麻醉—苏醒、苏醒—深麻醉:无符合条件的脑区激活。
结论
丙泊酚浅麻醉时,只有顶叶部分脑区的激活程度随ESC变化而变化,提示浅麻醉激活的脑区个体差异较大,共同的激活脑区较少。深麻醉时,左岛叶,左颞叶,右颞叶的激活程度随ESC变化而变化,提示这些区域可能是丙泊酚麻醉的作用靶位。浅麻醉—深麻醉激活的脑区较多,颞叶、岛叶、边缘叶、基底核均有脑区激活,提示这些脑区可能与意识消失有关。苏醒期无符合条件的脑区激活,提示苏醒期的激活脑区个体差异较大,本试验没有探寻到共同的苏醒相关脑区。
第二部分丙泊酚遗忘作用的加工分离程序研究和功能性磁共振成像研究
目的
应用加工分离程序(PDP)和BOLD-fMRI,观察丙泊酚遗忘作用在人脑中枢的敏感部位,探寻外显记忆和内隐记忆的处理脑区。
方法
20名男性健康志愿者随机分为2组:浅麻醉组(BIS 60～80)和深麻醉组(BIS 40～60)。先行预试验,靶控输注丙泊酚。浅麻醉组,计算预试验中每个受试者BIS 80点和BIS 60点的丙泊酚效应室浓度(ESC)的平均数,以此作为该受试者的目标ESC。深麻醉组,计算BIS 60点和BIS 40点的丙泊酚ESC的平均数,以此作为目标ESC。预试验后1～2周内进行fMRI研究。采用心理学界广泛应用的PDP,该方法能良好地区分内隐记忆和外显记忆。扫描序列为:结构像+清醒听词扫描+麻醉听词扫描,采用组块设计:时间10min45s=45s空白+[(0.5s读词+1.5s空白)×20词+20s空白]×10遍。记录扫描期间监护仪数值,以及扫描前后OAA/S评分。PDP成绩,采用SPSS 13.0统计学软件进行处理和分析。使用SPM2,Matlab 6.5进行fMRI图像分析。
结果
1.①浅麻醉组(BIS 60～80,OAA/S 3分)麻醉中外显记忆与清醒比较显著降低(P＜0.05),麻醉中内隐记忆与清醒比较无显著差异。②深麻醉组(BIS40～60,OAA/S 1分)麻醉中外显记忆和内隐记忆与清醒比较均显著降低(P＜0.05)。2.①浅麻醉组麻醉听词所激活的脑区为两侧颞上回。②深麻醉组麻醉听词所激活的脑区主要为右顶下小叶、颞上回、颞中回和岛叶。③浅麻醉组(清醒听词—麻醉听词)所激活的脑区较多,为两侧额叶、顶叶、颞叶和左枕叶、左基底核。④深麻醉组(清醒听词—麻醉听词)所激活的脑区为,左丘脑、中央前回、前扣带回和右基底核。
结论
根据PDP成绩,丙泊酚浅麻醉时,麻醉中无明显外显记忆,但存在内隐记忆。丙泊酚深麻醉时,麻醉中无明显外显记忆和内隐记忆。浅麻醉组(清醒听词—麻醉听词)所激活的脑区较多,以两侧额叶、颞叶、顶叶和左枕叶为著,结合PDP成绩,提示这些脑区可能与外显记忆相关。深麻醉组(清醒听词—麻醉听词)所激活的脑区为,左丘脑、额叶、边缘叶和右基底核的部分脑区,结合PDP成绩,提示这些脑区可能与外显记忆和内隐记忆相关。
Part 1 Bispectral index study and functional magnetic resonance imaging study in the anesthetic effect of propofol
Objective
Using the bispectral index monitoring(BIS) and Blood oxygenation level-dependent functional magnetic resonance imaging(BOLD-fMRI) technology,to investigate specific brain regions related to anesthetic effect of propofol.
Methods
20 healthy male volunteers participated in the study,randomly allocated to 2 groups:light anesthesia group(group L)(BIS 60～80) or deep anesthesia group(group D)(BIS 40～60).Propofol was administrated by target controlled infusion system in pilot study.The target effect site concentration (ESC)of propofol in group L was defined as the average of the ESC in BIS 80 and BIS 60.The target ESC in group D was defined as the average of the ESC in BIS 60 and BIS 40.FMRI study proceeded from 1 to 2 weeks after pilot study.FMRI examinations were conducted to obtain the following sequences: structure imaging,anesthesia sequence(event-related design:15min= baseline scan 4min+infusion scan about 9min+balance scan about 2min). Recovery sequence(event-related design:15min=balance scan 4min+stop infusion scan 11min) proceeded only in group D.The monitoring data were recorded during the scanning and the OAA/S were recorded before and after each sequence.FMRI data processing is carried out with the SPM2 and Matlab 6.5 software package.
Results
①Activated brain region of propofol anesthesia in group L(BIS 60～80, OAA/S 3) was observed only in left inferior parietal lobule.②Activated brain regions of propofol anesthesia in group D(BIS 40～60,OAA/S 1) were observed in left insula and superior temporal gyrus and right middle temporal gyrus.③Activated brain regions of low anesthesia＞deep anesthesia were observed in bilateral insula,temporal lobe and limbic lobe and left basal nucleus and midbrain.④Activated brain region of deep anesthesia＞low anesthesia,recovery,deep anesthesia＞recovery,recovery＞deep anesthesia were all null.
Conclusion
Activation gradient of left inferior parietal lobule in low anesthesia varies with propofol ESC,which indicates that low anesthesia affects different brain regions in different volunteer,and common active brain regions are seldom. Activation gradient of left insula and bilateral temporal lobe in deep anesthesia vary with propofol ESC,which indicates that these regions are likely the targets of anesthetic action of propofol.No common active brain region was observed in recovery,which indicates large individual difference of active brain region during recovery.
Part 2 Process dissociation procedure study and functional magnetic resonance imaging study in the amnesic effect of propofol
Objective
Using the Process dissociation procedure(PDP) and Blood oxygenation level-dependent functional magnetic resonance imaging(BOLD-fMRI) technology,to investigate specific brain regions related to amnesic effect of propofol,and to explore processing brain regions of explicit and implicit memory.
Methods
20 healthy male volunteers participated in the study,randomly allocated to 2 groups:light anesthesia group(group L)(BIS 60～80) or deep anesthesia group(group D)(BIS 40～60).Propofol was administrated by target controlled infusion system in pilot study.The target effect site concentration (ESC) of propofol in group L was defined as the average of the ESC in BIS 80 and BIS 60.The target ESC in group D was defined as the average of the ESC in BIS 60 and BIS 40.FMRI study proceeded from 1 to 2 weeks after pilot study.PDP was used to estimate implicit and explicit memory for words presented during awake and anesthesia.FMRI examinations were conducted to obtain the following sequences:structure imaging,awake word sequence and anesthesia word sequence.Block design was applied as "10min45s=45s baseline+[(0.5s word stimulation+1.5s silence)×20+20s silence]".The monitoring data were recorded during the scanning and the OAA/S were recorded before and after each sequence.PDP data processing is carried out with SPSS 13.0 software package.FMRI data processing is carried out with the SPM2 and Matlab 6.5 software package.
Results
1.①Explicit memory during anesthesia period significantly decreased compared with awake period in group L(BIS 60～80,OAA/S 3),while implicit memory did not differ between anesthesia and awake period.②Explicit memory and implicit memory during anesthesia period both significantly decreased compared with awake period in group D(BIS 40～60,OAA/S 1). 2.①Active brain regions of word stimulation during anesthesia period in group L were observed in bilateral superior temporal gyrus.②Active brain regions of word stimulation during anesthesia period in group D were observed in right inferior parietal lobule,superior temporal gyrus,middle temporal gyrus and insula.③Active brain regions of awake word＞anesthesia word in group L were mainly observed in bilateral frontal lobe,parietal lobe and temporal lobe and left occipital lobe and basal nucleus.④Active brain regions of awake word＞anesthesia word in group D were observed in left thalamus,precentral gyrus,anterior cingulate and right basal nucleus.
Conclusion
According to PDP estimates,only explicit memory disappears during light anesthesia,but implicit memory still exists.Explicit memory and implicit memory are both disappeared during deep anesthesia.Active brain regions of awake word＞anesthesia word in group L were mainly observed in bilateral frontal lobe,temporal lobe and parietal lobe and left occipital lobe.According to PDP estimates,these regions are likely related to explicit memory processing. Active brain regions of awake word＞anesthesia word in group D were observed in left thalamus,frontal lobe and limbic lobe and right basal nucleus. According to PDP estimates,these regions are likely related to explicit and implicit memory.
目的
应用脑电双频谱指数监测(BIS)和血氧水平依赖的功能性磁共振成像(BOLD-fMRI),观察丙泊酚麻醉作用在人脑中枢的敏感部位。
方法
20名男性健康志愿者随机分为2组:浅麻醉组(BIS 60～80)和深麻醉组(BIS 40～60)。先行预试验,靶控输注丙泊酚。浅麻醉组,计算预试验中每个受试者BIS 80点和BIS 60点的丙泊酚效应室浓度(ESC)的平均数,以此作为该受试者的目标ESC。深麻醉组,计算BIS 60点和BIS 40点的丙泊酚ESC的平均数,以此作为目标ESC。预试验后1～2周内进行fMRI研究。扫描序列为:结构像+麻醉扫描(事件相关设计:时间15min=4min空白扫描+约9min输注丙泊酚扫描+约2min达目标ESC后扫描),深麻醉组还需进行苏醒扫描(事件相关设计:时间15min=4min目标丙泊酚ESC扫描+11min停止输注后扫描)。记录扫描期间监护仪数值,以及扫描前后观察者觉醒/镇静评分(OAA/S)评分。使用SPM2、Matlab 6.5软件进行fMRI图像分析。
结果
①浅麻醉组(BIS 60～80,OAA/S 3分)丙泊酚麻醉所激活的脑区,仅有左顶下小叶区。②深麻醉组(BIS 40～60,OAA/S 1分)丙泊酚麻醉所激活的脑区,为左岛叶,左颞上回,右颞中回。③浅麻醉—深麻醉所激活的脑区较多,两侧岛叶、颞叶、边缘叶和左基底核、中脑均有脑区激活。④深麻醉—浅麻醉、苏醒期、深麻醉—苏醒、苏醒—深麻醉:无符合条件的脑区激活。
结论
丙泊酚浅麻醉时,只有顶叶部分脑区的激活程度随ESC变化而变化,提示浅麻醉激活的脑区个体差异较大,共同的激活脑区较少。深麻醉时,左岛叶,左颞叶,右颞叶的激活程度随ESC变化而变化,提示这些区域可能是丙泊酚麻醉的作用靶位。浅麻醉—深麻醉激活的脑区较多,颞叶、岛叶、边缘叶、基底核均有脑区激活,提示这些脑区可能与意识消失有关。苏醒期无符合条件的脑区激活,提示苏醒期的激活脑区个体差异较大,本试验没有探寻到共同的苏醒相关脑区。
第二部分丙泊酚遗忘作用的加工分离程序研究和功能性磁共振成像研究
目的
应用加工分离程序(PDP)和BOLD-fMRI,观察丙泊酚遗忘作用在人脑中枢的敏感部位,探寻外显记忆和内隐记忆的处理脑区。
方法
20名男性健康志愿者随机分为2组:浅麻醉组(BIS 60～80)和深麻醉组(BIS 40～60)。先行预试验,靶控输注丙泊酚。浅麻醉组,计算预试验中每个受试者BIS 80点和BIS 60点的丙泊酚效应室浓度(ESC)的平均数,以此作为该受试者的目标ESC。深麻醉组,计算BIS 60点和BIS 40点的丙泊酚ESC的平均数,以此作为目标ESC。预试验后1～2周内进行fMRI研究。采用心理学界广泛应用的PDP,该方法能良好地区分内隐记忆和外显记忆。扫描序列为:结构像+清醒听词扫描+麻醉听词扫描,采用组块设计:时间10min45s=45s空白+[(0.5s读词+1.5s空白)×20词+20s空白]×10遍。记录扫描期间监护仪数值,以及扫描前后OAA/S评分。PDP成绩,采用SPSS 13.0统计学软件进行处理和分析。使用SPM2,Matlab 6.5进行fMRI图像分析。
结果
1.①浅麻醉组(BIS 60～80,OAA/S 3分)麻醉中外显记忆与清醒比较显著降低(P＜0.05),麻醉中内隐记忆与清醒比较无显著差异。②深麻醉组(BIS40～60,OAA/S 1分)麻醉中外显记忆和内隐记忆与清醒比较均显著降低(P＜0.05)。2.①浅麻醉组麻醉听词所激活的脑区为两侧颞上回。②深麻醉组麻醉听词所激活的脑区主要为右顶下小叶、颞上回、颞中回和岛叶。③浅麻醉组(清醒听词—麻醉听词)所激活的脑区较多,为两侧额叶、顶叶、颞叶和左枕叶、左基底核。④深麻醉组(清醒听词—麻醉听词)所激活的脑区为,左丘脑、中央前回、前扣带回和右基底核。
结论
根据PDP成绩,丙泊酚浅麻醉时,麻醉中无明显外显记忆,但存在内隐记忆。丙泊酚深麻醉时,麻醉中无明显外显记忆和内隐记忆。浅麻醉组(清醒听词—麻醉听词)所激活的脑区较多,以两侧额叶、颞叶、顶叶和左枕叶为著,结合PDP成绩,提示这些脑区可能与外显记忆相关。深麻醉组(清醒听词—麻醉听词)所激活的脑区为,左丘脑、额叶、边缘叶和右基底核的部分脑区,结合PDP成绩,提示这些脑区可能与外显记忆和内隐记忆相关。
Part 1 Bispectral index study and functional magnetic resonance imaging study in the anesthetic effect of propofol
Objective
Using the bispectral index monitoring(BIS) and Blood oxygenation level-dependent functional magnetic resonance imaging(BOLD-fMRI) technology,to investigate specific brain regions related to anesthetic effect of propofol.
Methods
20 healthy male volunteers participated in the study,randomly allocated to 2 groups:light anesthesia group(group L)(BIS 60～80) or deep anesthesia group(group D)(BIS 40～60).Propofol was administrated by target controlled infusion system in pilot study.The target effect site concentration (ESC)of propofol in group L was defined as the average of the ESC in BIS 80 and BIS 60.The target ESC in group D was defined as the average of the ESC in BIS 60 and BIS 40.FMRI study proceeded from 1 to 2 weeks after pilot study.FMRI examinations were conducted to obtain the following sequences: structure imaging,anesthesia sequence(event-related design:15min= baseline scan 4min+infusion scan about 9min+balance scan about 2min). Recovery sequence(event-related design:15min=balance scan 4min+stop infusion scan 11min) proceeded only in group D.The monitoring data were recorded during the scanning and the OAA/S were recorded before and after each sequence.FMRI data processing is carried out with the SPM2 and Matlab 6.5 software package.
Results
①Activated brain region of propofol anesthesia in group L(BIS 60～80, OAA/S 3) was observed only in left inferior parietal lobule.②Activated brain regions of propofol anesthesia in group D(BIS 40～60,OAA/S 1) were observed in left insula and superior temporal gyrus and right middle temporal gyrus.③Activated brain regions of low anesthesia＞deep anesthesia were observed in bilateral insula,temporal lobe and limbic lobe and left basal nucleus and midbrain.④Activated brain region of deep anesthesia＞low anesthesia,recovery,deep anesthesia＞recovery,recovery＞deep anesthesia were all null.
Conclusion
Activation gradient of left inferior parietal lobule in low anesthesia varies with propofol ESC,which indicates that low anesthesia affects different brain regions in different volunteer,and common active brain regions are seldom. Activation gradient of left insula and bilateral temporal lobe in deep anesthesia vary with propofol ESC,which indicates that these regions are likely the targets of anesthetic action of propofol.No common active brain region was observed in recovery,which indicates large individual difference of active brain region during recovery.
Part 2 Process dissociation procedure study and functional magnetic resonance imaging study in the amnesic effect of propofol
Objective
Using the Process dissociation procedure(PDP) and Blood oxygenation level-dependent functional magnetic resonance imaging(BOLD-fMRI) technology,to investigate specific brain regions related to amnesic effect of propofol,and to explore processing brain regions of explicit and implicit memory.
Methods
20 healthy male volunteers participated in the study,randomly allocated to 2 groups:light anesthesia group(group L)(BIS 60～80) or deep anesthesia group(group D)(BIS 40～60).Propofol was administrated by target controlled infusion system in pilot study.The target effect site concentration (ESC) of propofol in group L was defined as the average of the ESC in BIS 80 and BIS 60.The target ESC in group D was defined as the average of the ESC in BIS 60 and BIS 40.FMRI study proceeded from 1 to 2 weeks after pilot study.PDP was used to estimate implicit and explicit memory for words presented during awake and anesthesia.FMRI examinations were conducted to obtain the following sequences:structure imaging,awake word sequence and anesthesia word sequence.Block design was applied as "10min45s=45s baseline+[(0.5s word stimulation+1.5s silence)×20+20s silence]".The monitoring data were recorded during the scanning and the OAA/S were recorded before and after each sequence.PDP data processing is carried out with SPSS 13.0 software package.FMRI data processing is carried out with the SPM2 and Matlab 6.5 software package.
Results
1.①Explicit memory during anesthesia period significantly decreased compared with awake period in group L(BIS 60～80,OAA/S 3),while implicit memory did not differ between anesthesia and awake period.②Explicit memory and implicit memory during anesthesia period both significantly decreased compared with awake period in group D(BIS 40～60,OAA/S 1). 2.①Active brain regions of word stimulation during anesthesia period in group L were observed in bilateral superior temporal gyrus.②Active brain regions of word stimulation during anesthesia period in group D were observed in right inferior parietal lobule,superior temporal gyrus,middle temporal gyrus and insula.③Active brain regions of awake word＞anesthesia word in group L were mainly observed in bilateral frontal lobe,parietal lobe and temporal lobe and left occipital lobe and basal nucleus.④Active brain regions of awake word＞anesthesia word in group D were observed in left thalamus,precentral gyrus,anterior cingulate and right basal nucleus.
Conclusion
According to PDP estimates,only explicit memory disappears during light anesthesia,but implicit memory still exists.Explicit memory and implicit memory are both disappeared during deep anesthesia.Active brain regions of awake word＞anesthesia word in group L were mainly observed in bilateral frontal lobe,temporal lobe and parietal lobe and left occipital lobe.According to PDP estimates,these regions are likely related to explicit memory processing. Active brain regions of awake word＞anesthesia word in group D were observed in left thalamus,frontal lobe and limbic lobe and right basal nucleus. According to PDP estimates,these regions are likely related to explicit and implicit memory.
引文
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8. Kerssens C, Sebel PS. BIS and memory function during anesthesia,Awareness during aensthesia. Edited by Ghoneim MM.Woburn,MA,Butterworth-Heinemann,2001,p 103-116
9. Kerssens C, Ouchi T, Sebel PS. No evidence of memory function during anesthesia with propofol or isoflurane with close control of hypnotic state.Anesthesiology, 2005, 102:57-62
10. Struys MM, Jensen EW, Smith W, et al. Performance of the ARX-derived auditory evoked potential index as an indicator of anesthetic depth: a comparison with bispectral index and hemodynamic measures during propofol administration. Anesthesiology, 2002, 96:803-816
1.Jacoby LL.A process dissociation framework:Separating automatic from intentional uses of memory.J Mem Lang,1991,30:513-541
2.Lubke GH,Kerssens C,Phaf H,et al.Dependence of explicit and implicit memory on hypnotic state in trauma patients.Anesthesiology,1999,90:670-680
3.Stapleton CL,Andrade J.An investigation of learning during propofol sedation and anesthesia using the process dissociation procedure.Anesthesiology,2000,93:1418-1425
4.Wang Y,Yue Y,Sun YH,et al.Can bispectral index or auditory evoked potential index predict implicit memory during propofol-induced sedation?Chin Med J,2006,119:894-898
5.Kerssens C,Takashi O,Peter S,et alo No Evidence of Memory Function during Anesthesia with Propofol or Isoflurane with Close Control of Hypnotic State.Anesthesiology,2005,102:57-62
6.Kerssens C,Lubke GH,Klein J,et al.Memory function during propofol and alfentanil anesthesia:predictive value of individual differences.Anesthesiology,2002,97:382-389
7.Kerssens C,Sebel PS.BIS and memory function during anesthesia,Awareness during aensthesia.Edited by Ghoneim MM.Woburn,MA,Butterworth-Heinemann,2001,p 103-116
8.岳云.麻醉与记忆.临床麻醉学杂志,2001,17:228-223
9.Buckner RL,Koutstaal W.Functional neuroimaging studies of encoding,priming,and explicit memory retrieval.Proc Natl Acad Sci USA,1998,95:891-898.Review.
10.朱湘如,刘昌.前扣带回功能的冲突监测理论.心理科学进展,2005,13:767-773
1. Barinaga M. New imaging methods provide a better view into the brain.Science, 1997, 276:1974-1976
2. Nofzinger EA, Mintun MA, Wiseman M, et al. Forebrain activation in REM sleep: an FDG PET study. Brain Res, 1997,770:192-201
3. Herscovitch P. Can [150] water be used evaluate drugs? J Clin Pharmacol, 2001,41:S11-S20
4. Grasby P, Malizia A, Bench C. Psychopharmacology in vivo neurochemistry and pharmacology. Br Med Bull, 1996, 52:513-526
5. Richardson MP, Friston KJ, Sisodiya SM, et al. Cortical grey matter and benzodiazepine receptors in malformations of cortical development. A voxel-based comparison of structural and functional imaging data. Brain,1997,120:1961-1973
6. Kety SS. The theory and applications of the exchange of inert gas at the lungs and tissues. Pharmacol Rev, 1951,3:1-41
7. Sokoloff L. Relation between physiological function and energy metabolism in the central nervous system. J Neurochem,1977,29:13-26
8. Sokoloff L. Relationships among local functional activity, energy metabolism, and blood flow in the central nervous system. Fed Proc.1981,40:2311-2231
9. Duncan JS. Positron emission tomography receptor studies. Adv Neurol,1999,79:893-899
10. Alkire MT. Quantitative EEG correlations with brain glucose metabolic rate during anesthesia in volunteers. Anesthesiology, 1998, 89:323-333
11. Alkire MT, Pomfrett CJ, Haier RJ, et al. Functional brain imaging during halothane anesthesia in humans: effects of halothane on global and regional cerebral glucose metabolism. Anesthesiology, 1999,90:701-709
12. Alkire MT, Haier RJ, Shah NK, et al. Positron emission tomography study regional cerebral metabolism in humans during isoflurane anesthesia. Anesthesiology, 1997,86:549-557
13. Alkire MT, Haier RJ, Barker SJ, et al. Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography. Anesthesiology, 1995,82:393-403
14. Alkire MT, Haier RJ, Fallon JH. Toward a unified theory of narcosis: brain imaging evidence for thalamocortical switch as the neurophysiologic basis of anesthetic-induced unconsciousness. Conscious Cogn, 2000, 9:370-386
15. Kaisti KK, Metsahonkala L, Teras M, et al. Effects of surgical levels of propofol and sevoflurane anesthesia on cerebral blood flow in healthy subjects studied with positron emission tomography. Anesthesiology,2002,96:1358-1370
16. Fiset P, Paus T, Daloze T, et al. Brain mechanisms of propofol-induced loss of consciousness in humans: a positron emission tomographic study.J Neurosci, 1999, 19:5506-5513
17. Bonhomme V, Fiset P, Meure P, et al. Propofol anesthesia and cerebral blood flow changes elicited by vibrotactile stimulation: a positron emission tomography study. J Neurophydiol, 2001,85:1299-1308
18. Reinsel rA, Veselis RA, Beattie BJ, et al. Midazolam changes cerebral blood flow in discrete brain regions. Anesthesiology,1997,87:1106-1117
19. Paus T. Functional anatomy of arousal and attention systems in the human brain. Prog Brain Res, 2000,126:65-77
20. Veselis RA, Reinsel R, Feshenko V, et al. Dose related decrease in rCBF in R and L prefrontal cortices (PFC) during memory impairment with midazolam and propofol. Neuroimage, 2001, 6:13-18
21. Gyulai FE, Minrun MA, firestone LL. Dose-dependent enhancement of in vivo GABA(A) — benzodiazepine receptor binding by isoflurane.Anesthesiology, 2001,95:585-593
22. Alkire MT, Haier BJ. Correlating in vivo anaesthetic effects with ex vivo receptor density data supports a A\GABAergic mechanism of action for propofol, but not for isoflurane. Br J Anaesth, 2001, 86:618-626
23. Forster BB, Mackay AL, Whittall KP, et al. Functional magnetic resonance imaging the basics of blood-oxygen-level-dependent imaging. Can Assoc Radiol, 1998,49:320-329
24. Bandettini PA, Wong EC, Hinks RS, et al. Time course EPI of human brain function during task activation. Magn Reson Med,1992, 25:390-397
25. Buxton RB, Wong EC, Frank LR. Dynamics of blood flow and oxygenation changes during brain activation: the balloon model. Magn Reson Med, 1998, 39: 855-864
26. Friston KJ, Mechelli,Turner R, et al. Nonlinear responses in fMRI: the balloon model, Volterra kernels and other hemodynamics. Neuroimaging,2000,12:468-477
27. Duyn JH, Mattay VS, Sexton RH, et al. 3-dimensional functional imaging of human brain using echo-shifted FLASH MRI. Magn Reson Med, 1994,32:150-155
28. Senior C, Barnes J, Giampietro V, et al. The functional neuroanatomy of implicit-motion perception or representational momentum. Curr Biol, 2000,10:16-22
29. Bucher RL, Goodman J, Burock M. Functional-anatomic correlates of object priming in human revealed by rapid presentation event- related fMRI. Neuron, 1998, 20:285-296
30. Antognini JF, Buonocore MH, Disbrow EA, et al. Isoflurane anesthesia blunts cerebral responses to noxious and innocuous stimuli: a fMRI study.Life Sci, 1997, 61:PL349-354
31. Heinke W, Schwarzbauer C. Subanesthetic isoflurane affects task-induced brain activation in a highly specific manner. Anesthesiology,2001,95:583-593
32. Heinke W, Schwarzbauer C. In vivo imaging of anasthetic action in humans: approaches with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). Br J Anaesth, 2002, 89: 112-122
33. John ER. The neurophysics of consciousness. Brain Res Rev, 2002, 39:1-28
34. Bagary M, Fluck E, File SE, et al. Is benzodiazepine-induced amnesia due to deactivation of the left prefrontal cortex. Psychopharmacology,2000,150:292-299
35. Stabemack C, Zhang Y, Sonner JM, et al. Thiopental produces immobility primarily by supraspinal actions in rats. Anesth Analg, 2005,100:128-136
36. Koblin DD, Harris RA, Kendig JJ, et al. Hypothesis: inhaled anesthetics produce immobility and amnesia by different mechanisms at different sites. Anesth Analg, 1997, 84: 915-918
2. Roizen MR Cost-effective preoperative laboratory testing. JAMA,271:319, 1994. American Medical Association
3. Practice guidelines for postanesthetic care: a report by the American Society of Anesthesiologists Task Force on Postanesthetic Care.Anesthesiology, 2002,96:742-752
4. Scott RP, Saunders DA, Norman J. Propofol: clinical strategies for preventing the pain of injection. Anaesthesia, 1988,43:492-494
5. Chemik DA, Gillings D, Lainer H, et al. Validity and reliability of the Observer's Assessment of Alertness/Sedation scale: Study with intraveneous midazolam. J Clin psychopharmacol,1990,10:244-251
6. Aldrete JA. The post-anesthesia recovery score revisited. J Clin Anesth,1995,7:89-91
7. Wang Y, Yue Y, Sun YH, et al. Can bispectral index or auditory evoked potential index predict implicit memory during propofol-induced sedation?Chin Med J, 2006,119:894-898
8. Kerssens C, Sebel PS. BIS and memory function during anesthesia,Awareness during aensthesia. Edited by Ghoneim MM.Woburn,MA,Butterworth-Heinemann,2001,p 103-116
9. Kerssens C, Ouchi T, Sebel PS. No evidence of memory function during anesthesia with propofol or isoflurane with close control of hypnotic state.Anesthesiology, 2005, 102:57-62
10. Struys MM, Jensen EW, Smith W, et al. Performance of the ARX-derived auditory evoked potential index as an indicator of anesthetic depth: a comparison with bispectral index and hemodynamic measures during propofol administration. Anesthesiology, 2002, 96:803-816
1.Jacoby LL.A process dissociation framework:Separating automatic from intentional uses of memory.J Mem Lang,1991,30:513-541
2.Lubke GH,Kerssens C,Phaf H,et al.Dependence of explicit and implicit memory on hypnotic state in trauma patients.Anesthesiology,1999,90:670-680
3.Stapleton CL,Andrade J.An investigation of learning during propofol sedation and anesthesia using the process dissociation procedure.Anesthesiology,2000,93:1418-1425
4.Wang Y,Yue Y,Sun YH,et al.Can bispectral index or auditory evoked potential index predict implicit memory during propofol-induced sedation?Chin Med J,2006,119:894-898
5.Kerssens C,Takashi O,Peter S,et alo No Evidence of Memory Function during Anesthesia with Propofol or Isoflurane with Close Control of Hypnotic State.Anesthesiology,2005,102:57-62
6.Kerssens C,Lubke GH,Klein J,et al.Memory function during propofol and alfentanil anesthesia:predictive value of individual differences.Anesthesiology,2002,97:382-389
7.Kerssens C,Sebel PS.BIS and memory function during anesthesia,Awareness during aensthesia.Edited by Ghoneim MM.Woburn,MA,Butterworth-Heinemann,2001,p 103-116
8.岳云.麻醉与记忆.临床麻醉学杂志,2001,17:228-223
9.Buckner RL,Koutstaal W.Functional neuroimaging studies of encoding,priming,and explicit memory retrieval.Proc Natl Acad Sci USA,1998,95:891-898.Review.
10.朱湘如,刘昌.前扣带回功能的冲突监测理论.心理科学进展,2005,13:767-773
1. Barinaga M. New imaging methods provide a better view into the brain.Science, 1997, 276:1974-1976
2. Nofzinger EA, Mintun MA, Wiseman M, et al. Forebrain activation in REM sleep: an FDG PET study. Brain Res, 1997,770:192-201
3. Herscovitch P. Can [150] water be used evaluate drugs? J Clin Pharmacol, 2001,41:S11-S20
4. Grasby P, Malizia A, Bench C. Psychopharmacology in vivo neurochemistry and pharmacology. Br Med Bull, 1996, 52:513-526
5. Richardson MP, Friston KJ, Sisodiya SM, et al. Cortical grey matter and benzodiazepine receptors in malformations of cortical development. A voxel-based comparison of structural and functional imaging data. Brain,1997,120:1961-1973
6. Kety SS. The theory and applications of the exchange of inert gas at the lungs and tissues. Pharmacol Rev, 1951,3:1-41
7. Sokoloff L. Relation between physiological function and energy metabolism in the central nervous system. J Neurochem,1977,29:13-26
8. Sokoloff L. Relationships among local functional activity, energy metabolism, and blood flow in the central nervous system. Fed Proc.1981,40:2311-2231
9. Duncan JS. Positron emission tomography receptor studies. Adv Neurol,1999,79:893-899
10. Alkire MT. Quantitative EEG correlations with brain glucose metabolic rate during anesthesia in volunteers. Anesthesiology, 1998, 89:323-333
11. Alkire MT, Pomfrett CJ, Haier RJ, et al. Functional brain imaging during halothane anesthesia in humans: effects of halothane on global and regional cerebral glucose metabolism. Anesthesiology, 1999,90:701-709
12. Alkire MT, Haier RJ, Shah NK, et al. Positron emission tomography study regional cerebral metabolism in humans during isoflurane anesthesia. Anesthesiology, 1997,86:549-557
13. Alkire MT, Haier RJ, Barker SJ, et al. Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography. Anesthesiology, 1995,82:393-403
14. Alkire MT, Haier RJ, Fallon JH. Toward a unified theory of narcosis: brain imaging evidence for thalamocortical switch as the neurophysiologic basis of anesthetic-induced unconsciousness. Conscious Cogn, 2000, 9:370-386
15. Kaisti KK, Metsahonkala L, Teras M, et al. Effects of surgical levels of propofol and sevoflurane anesthesia on cerebral blood flow in healthy subjects studied with positron emission tomography. Anesthesiology,2002,96:1358-1370
16. Fiset P, Paus T, Daloze T, et al. Brain mechanisms of propofol-induced loss of consciousness in humans: a positron emission tomographic study.J Neurosci, 1999, 19:5506-5513
17. Bonhomme V, Fiset P, Meure P, et al. Propofol anesthesia and cerebral blood flow changes elicited by vibrotactile stimulation: a positron emission tomography study. J Neurophydiol, 2001,85:1299-1308
18. Reinsel rA, Veselis RA, Beattie BJ, et al. Midazolam changes cerebral blood flow in discrete brain regions. Anesthesiology,1997,87:1106-1117
19. Paus T. Functional anatomy of arousal and attention systems in the human brain. Prog Brain Res, 2000,126:65-77
20. Veselis RA, Reinsel R, Feshenko V, et al. Dose related decrease in rCBF in R and L prefrontal cortices (PFC) during memory impairment with midazolam and propofol. Neuroimage, 2001, 6:13-18
21. Gyulai FE, Minrun MA, firestone LL. Dose-dependent enhancement of in vivo GABA(A) — benzodiazepine receptor binding by isoflurane.Anesthesiology, 2001,95:585-593
22. Alkire MT, Haier BJ. Correlating in vivo anaesthetic effects with ex vivo receptor density data supports a A\GABAergic mechanism of action for propofol, but not for isoflurane. Br J Anaesth, 2001, 86:618-626
23. Forster BB, Mackay AL, Whittall KP, et al. Functional magnetic resonance imaging the basics of blood-oxygen-level-dependent imaging. Can Assoc Radiol, 1998,49:320-329
24. Bandettini PA, Wong EC, Hinks RS, et al. Time course EPI of human brain function during task activation. Magn Reson Med,1992, 25:390-397
25. Buxton RB, Wong EC, Frank LR. Dynamics of blood flow and oxygenation changes during brain activation: the balloon model. Magn Reson Med, 1998, 39: 855-864
26. Friston KJ, Mechelli,Turner R, et al. Nonlinear responses in fMRI: the balloon model, Volterra kernels and other hemodynamics. Neuroimaging,2000,12:468-477
27. Duyn JH, Mattay VS, Sexton RH, et al. 3-dimensional functional imaging of human brain using echo-shifted FLASH MRI. Magn Reson Med, 1994,32:150-155
28. Senior C, Barnes J, Giampietro V, et al. The functional neuroanatomy of implicit-motion perception or representational momentum. Curr Biol, 2000,10:16-22
29. Bucher RL, Goodman J, Burock M. Functional-anatomic correlates of object priming in human revealed by rapid presentation event- related fMRI. Neuron, 1998, 20:285-296
30. Antognini JF, Buonocore MH, Disbrow EA, et al. Isoflurane anesthesia blunts cerebral responses to noxious and innocuous stimuli: a fMRI study.Life Sci, 1997, 61:PL349-354
31. Heinke W, Schwarzbauer C. Subanesthetic isoflurane affects task-induced brain activation in a highly specific manner. Anesthesiology,2001,95:583-593
32. Heinke W, Schwarzbauer C. In vivo imaging of anasthetic action in humans: approaches with positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). Br J Anaesth, 2002, 89: 112-122
33. John ER. The neurophysics of consciousness. Brain Res Rev, 2002, 39:1-28
34. Bagary M, Fluck E, File SE, et al. Is benzodiazepine-induced amnesia due to deactivation of the left prefrontal cortex. Psychopharmacology,2000,150:292-299
35. Stabemack C, Zhang Y, Sonner JM, et al. Thiopental produces immobility primarily by supraspinal actions in rats. Anesth Analg, 2005,100:128-136
36. Koblin DD, Harris RA, Kendig JJ, et al. Hypothesis: inhaled anesthetics produce immobility and amnesia by different mechanisms at different sites. Anesth Analg, 1997, 84: 915-918