异丙酚靶控输注对健康志愿者脑葡萄糖代谢的影响

目的 应用正电子发射断层扫描(PET)技术,比较健康志愿者在清醒和异丙酚靶控输注(FCI)致意识消失状态下大脑不同解剖结构间葡萄糖代谢的差异。方法 健康男性志愿者5名,分别在清醒和意识消失期作PET扫描。意识消失期以异丙酚效应室浓度(ECC)2.5μg/ml为初始浓度,以±0.2μg/ml浓度梯度调整志愿者意识状态至改良OAA/S1分,并维持此ECC至扫描结束。~(18)FDG10mci推注完毕开始计时,在0～4.5(T_1)、4.5～9.5(T_2)、9.5～29.5(T_3)、29.5～44.5(T_4)、44.5～59.5(T_5)、(59.5～74.5)min(T_6)6个时段进行扫描。数据重建后立体定向选取全脑、额叶、顶叶、颞叶、枕叶、尾状核、豆状核、丘脑、小脑等感兴趣区域(ROI),并将各ROI闪烁点计数转化为标准摄取值(SUV),比较意识消失期各ROI在各时段与清醒期SUV的差异及其降低百分比。结果 T_(1-6)时段随时间延长全脑和各ROI的SUV降低百分比逐渐增加。与全脑比较,枕叶T_6时段SUV降低百分比增加、豆状核T_(3-5)时段SUV降低百分比降低(P<0.05或0.01)。与丘脑比较,尾状核、豆状核T_(2～6)时段SUV降低百分比降低(P<0.05)。T_(3～6)时段意识消失期SUV明显低于清醒期(P<0.01)。两期主要皮质区、皮质下中枢及小脑SUV均随时间延长而增加,相同时段比较均无统计学意义。L_(4～6)时段,清     

PET分析丙泊酚对人脑葡萄糖能量代谢的影响

目的　应用正电子发射计算机体层显像(PET)技术,观察丙泊酚对人脑不同区域内葡萄糖能量代谢(CMGlu)的影响,探讨丙泊酚在人脑可能的作用部位。方法　健康志愿者 7 名,每位志愿者分别在清醒、丙泊酚 1 .5μg/ml(镇静)和 3 0μg/ml(意识消失)靶浓度状态下注射18氟脱氧葡萄糖(18F -FDG)显像剂,平衡后进行PET扫描。以清醒状态作为对照,通过靶控输注(TCI)丙泊酚使志愿者达到镇静和意识消失状态。结果　(1)与清醒状态比较,镇静状态下脑电双频指数(BIS)明显降低(P<0. 05),平均动脉压(MAP)、呼吸频率(RR)和心率(HR)等指标无显著性改变;而意识消失状态下,MAP、BIS降低,呼吸抑制,呼气末二氧化碳分压( PET CO2 )升高,均有显著性差异(P<0. 05)。(2)与清醒状态比较,镇静状态下全脑的CMGlu下降(18. 0±4. 0)%。CMGlu的下降在大脑皮质最为明显(P<0. 05)。CMGlu在丘脑、小脑、海马和桥脑等区域也有不同程度的降低,但与清醒状态比较,无显著性差异。意识消失状态下,全脑 CMGlu 与清醒状态比较显著下降了(34. 1±7 .0)%(P<0 .05),在丘脑、大脑皮质、小脑和海马等区域 CMGlu明显低于清醒状态(P<0 .05),其中丘脑降幅最大为(51. 5±5 .0)%。结论　丙泊酚麻醉可明显降低全脑能量代谢,低剂量的丙泊酚首先影响皮层区的能量代谢,     

异丙酚镇静对硬膜外麻醉患者大脑皮层不同区域的作用及对记忆的影响

目的探讨异丙酚镇静对硬膜外麻醉患者大脑皮层不同区域的作用及对记忆的影响, 分析内隐记忆消失时的脑电非线性参数近似熵界值。方法10例择期行腹部或下肢手术患者,采用硬膜外麻醉,术中持续输注异丙酚镇静,输注速率为6 mg·kg-1·h-1,监测异丙酚给药前后近似熵及近似熵脑电非线性地形图。应用分离加工测试方法,调查内隐记忆和外显记忆的成绩。常规监测血液动力学参数。结果与入室后相比,镇静后近似熵降低(P<0.05)。与镇静前相比,镇静后外显记忆和内隐记忆成绩均下降(P<0.05)。内隐记忆消失时数近似熵为0.55。通过近似熵脑电非线性地形图动态观察发现,异丙酚对大脑皮层各区域抑制顺序是:顶叶区、枕叶区→额叶区、颞叶区→全脑皮层;各脑区恢复顺序是:额叶区和颞叶区→顶叶区和枕叶区→全脑皮层。结论硬膜外麻醉患者应用异丙酚镇静,近似熵低于0.55时,内隐记忆消失。异丙酚对大脑皮层各区域的抑制和恢复有一定的规律。     

异丙酚对健康志愿者不同脑区神经递质水平的影响

目的评价异丙酚对健康志愿者不同脑区神经递质水平的影响,探讨异丙酚的全麻机制。方法健康志愿者10名,应用磁共振波谱分析(1H-MRS)技术,分别在清醒状态下行MRS扫描, 作为自身对照波谱;然后靶控输注异丙酚,效应室浓度达3．0μg·ml-1时进行第二次MRS扫描,采集波谱。MRS扫描采用点解析波谱序列(PRESS)。扫描选择的感兴趣区(VOI)包括皮层运动区、皮层感觉区、丘脑、海马和基底节区。以各波谱峰下面积计算N-乙酰基天门冬氨酸(NAA)、谷氨酸(Glu)、γ-氨基丁酸(GABA)、胆碱类化合物(Cho)和肌酸(Cr)水平的变化。结果与清醒状态比较,异丙酚效应室浓度达3．0μg·ml-1时,丘脑和海马区NAA水平,丘脑、海马和基底节区Glu水平,皮层运动区、皮层感觉区、丘脑、海马和基底节区Cho水平降低(P<0．05);皮层运动区、皮层感觉区、丘脑、海马和基底节区GABA水平升高(P<0．05);Cr水平在上述5个区域差异无统计学意义(P>0．05)。丘脑和海马 GABA变化率大于其他部位(P<0．05或0．01)。结论异丙酚麻醉对健康志愿者不同脑区NAA、Glu、 GABA、Cho等神经递质水平均有影响,其中GABA可能在异丙酚的全麻机制中发挥较为重要作用。     

应用SPECT研究地氟醚麻醉对人脑血流分布的影响

目的研究吸入不同浓度地氟醚麻醉下健康志愿者脑血流(CBF)分布的动态变化。方法选择9名志愿者,每位志愿者分别在清醒、吸入0.5和1.0MAC地氟醚后采用单光子发射计算机断层成像(SPECT)仪进行扫描,观察地氟醚麻醉下人局部脑血流(rCBF)的动态变化。结果全脑CBF计数在清醒时为127.5±23.1,吸入0.5MAC地氟醚麻醉后全脑CBF计数为130.8±25.4,吸入1.0MAC地氟醚后为128.8±22.9,三组间比较差异无显著意义;额叶、顶叶、颞叶、枕叶、中脑、小脑、丘脑、海马、基底核、扣带回和舌回等脑区rCBF计数差异也均无显著意义。结论在保持PETCO2和MAP稳定且在正常范围时,吸入地氟醚麻醉不影响人脑内血流量的分布。     

安氟醚麻醉下健康志愿者脑葡萄糖代谢的显像研究

目的应用正电子发射断层扫描技术(positronemissiontomography,PET),研究健康志愿者吸入不同浓度安氟醚麻醉时脑葡萄糖代谢(CMGlu)的改变。方法选择5名志愿者,每位志愿者分别做3次PET扫描,采用PHILIPSCPETPlus扫描仪及18氟标记的脱氧葡萄糖(18FDG)标记技术测定CMGlu,第1次在清醒状态下扫描作为对照,第2、3次分别吸入0.5MAC和1.0MAC安氟醚。结果与清醒时比较,吸入0.5MAC和1.0MAC安氟醚后全脑CMGlu显著降低(P<0.05,P<0.01)。吸入0.5MAC安氟醚麻醉后脑内各区CMGlu计数均显著降低(P<0.05),但以丘脑、扣带回、额叶、楔叶、楔前叶和桥脑更为显著(P<0.01);与0.5MAC时比较,1.0MAC时全脑及脑内各区CMGlu计数均进一步降低(P<0.05),但程度基本一致。结论全脑及脑内各区CMGlu在吸入安氟醚麻醉时均可显著降低,且程度与吸入安氟醚的浓度似乎相关。丘脑、扣带回、额叶、楔叶、楔前叶和桥脑等脑区对安氟醚更为敏感。     

异氟醚对健康志愿者脑葡萄糖代谢率的影响

目的 应用正电子发射断层扫描技术(PET),研究吸入不同浓度异氟醚麻醉对健康志愿者脑葡萄糖代谢率(CMRGlu)的影响。方法 选择8名志愿者,每位志愿者分别做三次PET扫描,采用MASEP CPET Plus扫描仪及18F-FDG标记技术测定CMRGIu,第一次在清醒状态下扫描作为对照(清醒组),第二、三次分别吸入0.5 MAC和1.0MAC异氟醚(分别为0.5MAC组和1.0MAC组)后进行。结果 清醒组全脑CMRGlu平均为(30.0±1.1)μmol·100mg-1·min-1,与清醒组比较,0.5MAC组降低全脑CMRGlu24%至(23.3±1.4)μmol·100 mg·min-1(P<0.05),1.0MAC组降低41％至(18.4±0.9)μmol·100mg-1·min-1(P<0.01);脑内各区葡萄糖代谢率(CMRGlu)均显著降低,而以丘脑、楔叶和扣带回降低更为显著(P<0.01);与0.5MAC组比较,1.0MAC组全脑及各脑区rCMRGu进一步降低(P<0.05)。结论 全脑及脑内各区葡萄糖代谢率在吸入异氟醚麻醉时均可显著降低,丘脑、楔叶和扣带回对吸入异氟醚麻醉更为敏感。     

BIS监测异丙酚复合瑞芬太尼全麻患儿麻醉深度的准确性

目的 评价脑电双频谱指数(BIS)监测异丙酚复合瑞芬太尼全麻患儿麻醉深度的准确性.方法 择期手术患儿60例,ASA Ⅰ或Ⅱ级,年龄3～8岁,体重14～40kg,随机分为4组(n=15),人室后开放手背静脉,稳定5 min.C组静脉输注0.9%生理盐水0.2 ml·kg-1·h-1;R1组、R2组和R3组分别静脉输注瑞芬太尼0.1、0.3或0.5 μg·kg-1·min-1,瑞芬太尼或生理盐水输注10 min开始靶控输注异丙酚,起始效应室浓度为1 μg/ml,逐渐递增至2、3、4μg/ml.分别于稳定5min、瑞芬太尼静脉输注10min、异丙酚效应室浓度达到l、2、3、4μg/ml稳定1 min及意识消失时记录BIS和警觉,镇静(OAA/S)评分;记录意识消失时间.采用logistic回归法计算意识消失时的BIS50、BIS95和意识消失时异丙酚的EC50、EC95.BIS与OAA/S评分、异丙酚效应室浓度作直线相关分析.结果 C组、R1.组、R2组和R3组BIS与OAA/S评分均呈正相关,r分别为0.89、0.90、0.87、0.82(P<0.05);BIS与异丙酚效应室浓度均呈负相关,r分别为-0.87、-0.90、-0.87、-0.92(P<0.05);与C组比较,其余3组患儿意识消失时异丙酚效应室浓度降低,意识消失时间缩短,R2组和R3组意识消失时BIS升高,BIS50和BIS95升高,异丙酚EC50和EC95降低(P<0.05);与R1组比较,R2组BIS50和BIS95升高,R3组异丙酚EC50和EC95降低(P<0.05).结论 瑞芬太尼复合异丙酚麻醉下,采用BIS监测患儿麻醉深度存在一定局限性.     

异丙酚对大鼠两侧脑半球各皮质脑电互近似熵的影响

目的 探讨异丙酚对大鼠两侧脑半球顶叶、额叶和枕叶皮质脑电互近似熵(C-ApEn)的影响.方法 雄性SD大鼠36只,体重300～350 g,随机分为3组(n=12),分别于左右顶叶(Ⅰ组)、额叶(Ⅱ组)和枕叶(Ⅲ组)埋置硬膜外电极,连续监测自发腩电.于大鼠清醒状态下连续记录20 min脑电图,取最后2 min的脑电图进行后期分析并记为基础值;然后静脉输注异丙酚,初始输注速率为400μg·kg~(-1)·min~(-1),每次递增100 μg·kg~(-1)·min~(-1),直至900μg·kg~(-1)·min~(-1),每个速率持续输注10 min,取最后2 min的脑电图进行后期分析,计算不同异丙酚输注速率时两侧脑半球的C-ApEn.于埋置电极前1周时测定不同异丙酚输注速率时大鼠翻正反射和夹尾反射消失情况.结果 所有大鼠异丙酚500～600μg·kg~(-1)·min~(-1)时翻正反射消失,800～900 μg·kg~(-1)·min~(-1)时夹尾反射消失.各组给予异丙酚后的C-ApEn均低于清醒状态时,且随异丙酚剂量的增加C-ApEn逐渐降低(P<0.05).结论 异丙酚可剂量依赖性地降低两侧脑半球顶叶、额叶和枕叶皮质的信息交流和联系.C-ApEn是与异丙酚麻醉效应相关的敏感的非线性腩电参数.     

七氟醚麻醉对脑葡萄糖能量代谢的影响

目的研究吸人不同浓度七氟醚对健康志愿者脑内葡萄糖能量代谢（CMGlu）的影响,探讨七氟醚在人脑可能的作用部位。方法选择健康志愿者10名,每人分别做三次正电子发射计算机体层扫描：第一次在清醒状态下扫描作为对照;第二、三次分别吸人0．5MAC和1．0MAC七氟醚。结果（1）与清醒状态比较,镇静状态下脑电双频指数（BIS）明显降低（P〈0．05）,MAP、RR和HR等指标无显著改变;而意识消失状态下,MAP、BIS显著降低,呼吸抑制,PgrCO2升高（P〈0．05）。（2）清醒时全脑内CMGlu计数为2268．3±91．2,吸入0．5MAC七氟醚麻醉后CMGlu计数降低至1875．9±86．2（P〈0．05）,降低17％;吸入1．0MAC七氟醚后CMGlu计数降低至1556．3±80．4（P〈0．01）。与清醒时比较,吸入0．5MAC麻醉后脑内各区CMGlu计数均显著降低（P〈0．05）,以丘脑、楔叶、楔前叶和扣带回cMGlu计数降低更为显著（P〈0．01）,分别降低46％、41％、42％和40％;吸人1．0MAC麻醉后,全脑及脑内各区CMGlu计数均进一步降低8％～11％（P〈0．05）。结论七氟醚麻醉可明显降低全脑及脑内各区葡萄糖代谢,且程度与吸入七氟醚的浓度相关。丘脑、楔叶、楔前叶和扣带回对吸入七氟醚麻醉更为敏感,可能是七氟醚麻醉在脑内作用的主要靶区。     

Neural mechanism of propofol anesthesia in severe depression: a positron emission tomographic study

BACKGROUND: The precise neural mechanisms of propofol anesthesia in humans are still unknown. The authors examined the acute effects of propofol on regional cerebral blood flow (rCBF) using positron emission tomography in patients with severe depression. METHODS: In six severely depressed patients (mean age, 55.0 yr) scheduled for electroconvulsive therapy, anesthetic levels were monitored by electroencephalography, and rCBF was serially quantified in the awake, sedated, and anesthetized states. The authors used high-resolution positron emission tomography with 15O-labeled water and statistical parametric mapping 99 for imaging and analysis of the data. RESULTS: Global cerebral blood flow showed sharp decreases from the awake level during the administration of propofol, decreasing 26.8% in the sedated state and 54.4% in the anesthetized state. Moreover, a dose effect was seen in both parietal cortices and the left lateral prefrontal region with larger regions of relative decrease in rCBF at higher propofol doses. At the higher dose, the values of rCBF in the pulvinar nucleus of the thalamus, the pontine tegmentum, and the cerebellar cortex were also affected. Meanwhile, there were few changes of relative rCBF in the basal frontal lobes during both sedated and anesthetized states. CONCLUSIONS: As in earlier studies using normal subjects, pronounced suppression in rCBF in the brain stem reticular formation, the thalamus, and the parietal association cortex occurred even in severely depressed patients. However, previously reported decreases in rCBF in the basal frontal lobe were absent in depressed patients.     

Neural Mechanism of Propofol Anesthesia in Severe Depression: A Positron Emission Tomographic Study

Background: The precise neural mechanisms of propofol anesthesia in humans are still unknown. The authors examined the acute effects of propofol on regional cerebral blood flow (rCBF) using positron emission tomography in patients with severe depression.

Methods: In six severely depressed patients (mean age, 55.0 yr) scheduled for electroconvulsive therapy, anesthetic levels were monitored by electroencephalography, and rCBF was serially quantified in the awake, sedated, and anesthetized states. The authors used high-resolution positron emission tomography with 15O-labeled water and statistical parametric mapping 99 for imaging and analysis of the data.

Results: Global cerebral blood flow showed sharp decreases from the awake level during the administration of propofol, decreasing 26.8% in the sedated state and 54.4% in the anesthetized state. Moreover, a dose effect was seen in both parietal cortices and the left lateral prefrontal region with larger regions of relative decrease in rCBF at higher propofol doses. At the higher dose, the values of rCBF in the pulvinar nucleus of the thalamus, the pontine tegmentum, and the cerebellar cortex were also affected. Meanwhile, there were few changes of relative rCBF in the basal frontal lobes during both sedated and anesthetized states.     

BIS和CSI监测不同效应室靶浓度异丙酚复合舒芬太尼患者镇静水平的准确性

目的 评价脑电双频谱指数(BIS)和麻醉深度指数(CSI)监测不同效应室靶浓度异丙酚复合舒芬太尼患者镇静水平的准确性.方法 外科手术患者90例,ASA Ⅰ或Ⅱ级,年龄20～49岁,体重45～70 kg,性别不限,随机分为6组(n=15):P1～3组分别靶控输注不同效应室靶浓度(2、4、6 μg/ml)异丙酚;SP1～3组分别靶控输注不同效应室靶浓度(2、4、6 μg/ml)异丙酚复合舒芬太尼.异丙酚初始效应室靶浓度为4 μg/ml,于气管插管后即刻,P1组和SP1组调整为2 μg/ml,P2组和SP2组调整为4 μg/ml,P3组和SP3组调整为6 μg/ml,20 min后SP1～3组经2～3 min静脉注射舒芬太尼0.7 μg/kg.于麻醉诱导前(T0)、气管插管前1 min(T1)、插管后30 s(T2)、15 min(T3)、30 min(T4)、35 min(T5)及40 min(T6)时记录HR、MAP、BIS和CSI.结果 P1～3组T3～6时组间比较BIS和CSI依次降低(P<0.05或0.01);SP1～3组T3～6时BIS和CSI组间比较依次降低(P<0.05);SP1组和SP2组T4～6时BIS和CSI分别较P1组和P2组降低(P<0.05或0.01);与P3组比较,SP3组T4～6时CSI降低(P<0.05),BIS差异无统计学意义(P0.05).结论 异丙酚效应室靶浓度2、4 μg/ml复合舒芬太尼时,CSI和BIS均可反映患者镇静水平;异丙酚效应室靶浓度6 μg/ml复合舒芬太尼时,仅CSI可反映患者镇静水平.     

反复注射异丙酚对新生大鼠认知功能的影响

目的 探讨反复注射异丙酚对新生大鼠认知功能的影响.方法 清洁级SD大鼠24只,7 d龄,12～16 g,雌雄各半,随机分为3组(n=8):对照组(C组)腹腔注射生理盐水7.5 ml/kg,1次/d,连续7 d;单次注射异丙酚组(P1组)腹腔注射生理盐水7.5 ml/kg,1次/d,连续6 d,第7天腹腔注射异丙酚75 mg/kg;反复注射异丙酚组(P2组)腹腔注射异丙酚75 mg/kg,1次/d,连续7 d.异丙酚给药结束后2周时采用水迷宫实验测试学习记忆功能,然后断头处死大鼠,取脑组织,采用高效液相色谱法测定皮层和海马谷氨酸、天冬氨酸、甘氨酸和7.氨基丁酸的含量.结果 与C组和P1组比较,P2组认知功能下降,海马天冬氨酸含量降低,皮层和海马谷氨酸含量降低,谷氨酸/γ-氨基丁酸比值下降(P＜0.05),皮层和海马甘氨酸和γ-氨基丁酸含量差异无统计学意义(P＞0.05).结论 反复注射异丙酚可导致新生大鼠远期认知功能减退,可能与脑内兴奋性氨基酸递质含量的降低有关.     

体外循环下异丙酚靶控输注系统的准确性

目的 评价体外循环下异丙酚靶控输注系统的准确性.方法 择期体外循环下行心脏瓣膜置换术患者20例,ASAⅡ或Ⅲ级,年龄25～64岁,体重50～70 kg.静脉注射咪达唑仑、芬太尼和维库溴铵行麻醉诱导,气管插管后机械通气.麻醉维持采用嵌入Tackley药代动力学参数的靶控输注系统输注异丙酚至术毕,血浆靶浓度为1μ/ml.于体外循环前(T1)、体外循环开始后1、5、10、20、40、60 min(T2-7)、体外循环结束后5、10 min(T8,9)时采集桡动脉血样3 ml,采用反相高效液相色谱法测定血浆异丙酚浓度,计算异丙酚靶控输注系统的偏离度、精确度、摆动度及分散度.结果 T1时异丙酚实测浓度高于血浆靶浓度(P<0.05),T2-4时异丙酚实测浓度与血浆靶浓度差异无统计学意义(P>0.05),T5-9时异丙酚实测浓度高于血浆靶浓度(P<0.05).异丙酚靶控输注系统的偏离度为21%、精确度为29%、摆动度为21%及分散度为-0.06%/h.结论 心脏手术患者体外循环时,采用嵌入Tackley药代动力学参数的异丙酚靶控输注系统的准确性超出临床可接受范围.     

Midazolam Changes Cerebral Blood Flow in Discrete Brain Regions: An H sub 2 sup 15 O Positron Emission Tomography Study

Background: Changes in regional cerebral blood flow (rCBF) determined with H215 O positron emission tomographic imaging can identify neural circuits affected by centrally acting drugs.

Methods: Fourteen volunteers received one of two midazolam infusions adjusted according to electroencephalographic response. Low or high midazolam effects were identified using post-hoc spectral analysis of the electroencephalographic response obtained during positron emission tomographic imaging based on the absence or presence of 14-Hz spindle activity. The absolute change in global CBF was calculated, and relative changes in rCBF were determined using statistical parametric mapping with localization to standard stereotactic coordinates.

Results: The low-effect group received 7.5 +/- 1.7 mg midazolam (serum concentrations, 74 +/- 24 ng/ml), and the high-effect group received 9.7 +/- 1.3 mg midazolam (serum concentrations, 129 +/- 48 ng/ml). Midazolam decreased global CBF by 12% from 39.2 +/- 4.1 to 34.4 +/- 6.1 ml [center dot] 100 g sup -1 [center dot] min sup -1 (P < 0.02 at a partial pressure of carbon dioxide of 40 mmHg). The rCBF changes in the low-effect group were a subset of the high-effect group. Decreased rCBF (P < 0.001) occurred in the insula, the cingulate gyrus, multiple areas in the prefrontal cortex, the thalamus, and parietal and temporal association areas. Asymmetric changes occurred, particularly in the low-effect group, and were more significant in the left frontal cortex and thalamus and the right insula. Relative rCBF was increased in the occipital areas.     

Propofol and thiopental do not interfere with regional cerebral blood flow response at sedative concentrations

BACKGROUND: Anesthetics may affect the regional cerebral blood flow (rCBF) response associated with increased brain activity in humans. rCBF was measured as auditory stimulus rate was increased during propofol and thiopental administration. METHODS: After informed consent, 10 right-handed male volunteer participants (aged 33.5 +/- 10.4 yr, weighing 74.5 +/- 8.4 kg) received thiopental (n = 4) or propofol (n = 6) intravenously at stepwise target concentrations of propofol 1.2 and 2.5-3, or thiopental 4 and 7-9 microg/ml, representing sedative and hypnotic drug concentrations. The latter made volunteers unresponsive to voice or mild stimulation. Quantitative positron emission tomographic brain images were obtained at 0, 20, and 40 auditory words per minute at each drug concentration. Using SPM99 analysis, 10-mm spherical regions of interest were identified by peak covariation of word rate with rCBF across all conditions and drug concentrations. Individual mean rCBF responses in these and primary auditory cortex (Heschl's gyri) were obtained. RESULTS: Significant increases in rCBF with auditory word rate occurred in temporal lobes bilaterally at baseline (significance, T = 4.95). There was no change in this response during sedation (T = 5.60). During unresponsiveness seven of 10 participants had a diminished response in the left temporal lobe (T = 3.18). Global CBF, corrected for changes in PCO2 (3% .mmHg PCO2), was reduced 15% by sedation and 27% during unresponsiveness. CONCLUSION: The presence of propofol or thiopental does not affect the rCBF response to increasing stimulus rate during consciousness. Thus, changes in rCBF activation patterns with sedative concentrations of these drugs represent effects on brain activity itself. The neuroanatomical targets of drug effect on memory and attention may be revealed by changes in rCBF patterns associated with these cognitive activities.     

射频消融辅助上气道手术患者瑞芬太尼、异丙酚联合局部麻醉的效果

目的 评价射频消融辅助上气道手术(CAUP)患者瑞芬太尼、异丙酚联合局部麻醉的效果.方法 拟在局麻下行CAUP手术的中、重度阻塞性睡眠呼吸暂停低通气综合征患者80例,年龄25～60岁,体重指数≤35 kg/m2,ASA Ⅰ或Ⅱ级,随机分为4组(n=20):生理盐水组(S组)、异丙酚组(P组)、瑞芬太尼组(R组)和异丙酚复合瑞芬太尼组(PR组).1%丁卡因咽部表面麻醉后,S组静脉输注生理盐水0.15 ml·kg-1·h-1,P组静脉输注异丙酚25μg·kg-1·min-1,R组静脉输注瑞芬太尼O.05μg·kg·min-1,PR组静脉输注异丙酚25μg·ks-1·min-1和瑞芬太尼0.05μg·kg-1·min-1.10 min后用含1:200 000肾上腺素的利多卡因行术野局部浸润麻醉.术中每5分钟采用Ramsay评分评价镇静程度;采用主诉疼痛分级(VRS)评价疼痛程度.S组VRS分级为Ⅲ级时为麻醉失败,其余3组VRS分级为Ⅲ级时,增加输注速率或静脉注射异丙酚10 mg或瑞芬太尼20μg;如出现Ramsay评分>3分或呼吸抑制(RR<8次/min或SpO2<95%),则为麻醉失败.于射频消融前和射频消融5 min时记录BP和HR.记录气道阻塞和呼吸暂停等不良反应的发生情况.结果 R组、PR组麻醉成功率(分别为90%、100%)高于s组和P组(分别为40%、65%)(P<0.05).与S组比较,射频消融5 min时P组SP、DP和HR差异无统计学意义(P>0.05),R组和PR组SP、DP和HR降低(P<0.05).4组不良反应发生率比较差异无统计学意义(P>O.05).结论 瑞芬太尼和异丙酚复合瑞芬太尼联合局部麻醉可安全、有效地用于患者射频消融辅助上气道手术.     

A neuroanatomical construct for the amnesic effects of propofol

BACKGROUND: This study was designed to identify neuroanatomical locations of propofol's effects on episodic memory by producing minimal and maximal memory impairment during conscious sedation. Drug-related changes in regional cerebral blood flow (rCBF) were located in comparison with rCBF increases during a simple word memory task. METHODS: Regional cerebral blood flow changes were assessed in 11 healthy volunteers using H215O positron emission tomography (PET) and statistical parametric mapping (SPM99) at 600 and 1,000 ng/ml propofol target concentrations. Study groups were based on final recognition scores of auditory words memorized during PET scanning. rCBF changes during propofol administration were compared with those during the word memory task at baseline. RESULTS: Nonoverlapping memory effects were evident: low (n = 4; propofol concentration 523 +/- 138 ng/ml; 44 +/- 13% decrement from baseline memory) and high (n = 7; 829 +/- 246 ng/ml; 87 +/- 6% decrement from baseline) groups differed in rCBF reductions primarily in right-sided prefrontal and parietal regions, close to areas activated in the baseline memory task, particularly R dorsolateral prefrontal cortex (Brodmann area 46; x, y, z = 51, 38, 22). The medial temporal lobe region exhibited relative rCBF increases. CONCLUSIONS: As amnesia becomes maximal, rCBF reductions induced by propofol occur in brain regions identified with working memory processes. In contrast, medial temporal lobe structures were resistant to the global CBF decrease associated with propofol sedation. The authors postulate that the episodic memory effect of propofol is produced by interference with distributed cortical processes necessary for normal memory function rather than specific effects on medial temporal lobe structures.     

Propofol and Thiopental Do Not Interfere with Regional Cerebral Blood Flow Response at Sedative Concentrations

Background: Anesthetics may affect the regional cerebral blood flow (rCBF) response associated with increased brain activity in humans. rCBF was measured as auditory stimulus rate was increased during propofol and thiopental administration.

Methods: After informed consent, 10 right-handed male volunteer participants (aged 33.5 +/- 10.4 yr, weighing 74.5 +/- 8.4 kg) received thiopental (n = 4) or propofol (n = 6) intravenously at stepwise target concentrations of propofol 1.2 and 2.5-3, or thiopental 4 and 7-9 [mu]g/ml, representing sedative and hypnotic drug concentrations. The latter made volunteers unresponsive to voice or mild stimulation. Quantitative positron emission tomographic brain images were obtained at 0, 20, and 40 auditory words per minute at each drug concentration. Using SPM99 analysis, 10-mm spherical regions of interest were identified by peak covariation of word rate with rCBF across all conditions and drug concentrations. Individual mean rCBF responses in these and primary auditory cortex (Heschl's gyri) were obtained.

Results: Significant increases in rCBF with auditory word rate occurred in temporal lobes bilaterally at baseline (significance, T = 4.95). There was no change in this response during sedation (T = 5.60). During unresponsiveness seven of 10 participants had a diminished response in the left temporal lobe (T = 3.18). Global CBF, corrected for changes in Pco2 (3% [middle dot]mmHg Pco2-1), was reduced 15% by sedation and 27% during unresponsiveness.