七氟醚麻醉下瑞芬太尼抑制小儿切皮反应的血浆靶浓度

目的 确定七氟醚麻醉下瑞芬太尼抑制小儿切皮时躯体和心血管反应的血浆靶浓度.方法 择期全麻手术小儿75例,年龄2～5岁,ASA Ⅰ级,随机均分为五组,七氟醚吸入诱导后,采用Minto药代动力学模型靶控输注瑞芬太尼,血浆靶浓度分别为1、2、3、4、5 ng/ml(R1～R5组),维持呼气末七氟醚浓度稳定在1.5%,15 min后开始切皮.切皮即刻,小儿发生体动为躯体反应阳性;MAP或HR较切皮前升高或增快＞15%为心血管反应阳性.Probit法计算瑞芬太尼抑制50%和95%患儿切皮即刻躯体和心血管反应的有效血浆靶浓度(Cp50和CP95).结果 五组瑞芬太尼抑制切皮时躯体反应有效构成比分别为0/15、5/15、12/15、15/15、15/15;抑制心血管反应有效构成比分别为0/15、2/15、8/15、13/15、14/15.结论 在1.5%七氟醚麻醉下,瑞芬太尼抑制2～5岁小儿切皮时躯体反应的Cp50及其95%可信区间为2.29(1.92～2.59)ng/ml,Cp95及其95%可信区间为3.53(3.02～5.03)ng/ml;抑制心血管反应的Cp50及其95%可信区间为2.89(2.46～3.29)ng/ml,Cp95及其95%可信区间为4.99(4.19～7.18)ng/ml.     

雷米芬太尼靶控输注抑制全麻拔管期心血管不良反应的剂量探讨

目的探讨雷米芬太尼靶控输注(TCI)拔管期有效抑制心血管反应的半数有效血浆浓度(EC50)。方法择期全麻下行腹腔镜胆囊切除术(LC)成人患者40例,按照序贯法TCI血浆浓度分别为0.6、0.8、1.0、1.2和1.4 ng/ml的雷米芬太尼,初始靶浓度为1.0 ng/ml,若患者拔管时SBP高于基础值的20%或HR快于100次/分,或拔管时出现呛咳、躁动,则下一例患者采用高一级浓度的雷米芬太尼TCI;反之则采用低一级浓度的雷米芬太尼TCI。计算全麻拔管期有效抑制心血管反应的雷米芬太尼EC50及其95%可信区间(CI)。结果TCI雷米芬太尼抑制心血管反应的EC50为1.03 ng/ml,其95%CI为0.97~1.09 ng/ml。结论LC全麻拔管期有效抑制心血管反应的雷米芬太尼EC50为1.03 ng/ml。     

靶控输注芬太尼复合异丙酚静脉麻醉的药效学

目的研究以血浆靶浓度(Ct)3μg/ml靶控输注(TCI)异丙酚时，50％和95％病人对切皮刺激无体动或心血管反应的芬太尼设定血浆靶浓度(Cp50和Cp95)及其量效关系。方法24例择期行全身麻醉手术的病人，ASAⅠ-Ⅱ级，年龄31—65岁，按芬太尼血浆靶浓度随机分为四组，每组6例。麻醉诱导时通过TCI系统使所有病人异丙酚血浆靶浓度达到和维持3μg/ml，使各组芬太尼的血浆靶浓度分别达到1．00、1．50、2．25、3．38ng/ml。观察和记录手术切皮刺激引起的体动反应和心血管反应。分别计算抑制切皮时体动反应和心血管反应的Cp50、Cp95，并建立对切皮刺激反应的芬太尼量-效关系曲线。结果切皮时体动无反应率随设定的芬太尼靶浓度(当异丙酚Ct=3μg/ml)增加而逐渐增高，病人对切皮刺激无体动反应的Cp50为1．84ng/ml，其95％可信区间为1．46—2．33ng/ml，相应的Cp9，为5．12ng/ml，靶浓度对数剂量(x)与体动无反应率的概率单位(Y)间的回归方程为：Y=2．45X 4．35。同样，病人心血管无反应率随设定的芬太尼靶浓度增加而逐渐增高,Cp50为2．67ng/ml，其95％可信区间为(1．96—3．62)ng/ml，相应的cp95为15．85ng/ml，靶浓度对数剂量(X)与心血管无反应率的概率单位(Y)间的回归方程为：Y=2．13X 4．09。结论靶控输注异丙酚(Ct=3μg／ml)复合芬太尼麻醉，设定芬太尼靶浓度至少为5．12ng/ml，切皮时可以达到满意的麻醉深度。     

七氟醚吸入诱导下瑞芬太尼抑制喉罩插入反应的半数有效血浆靶控浓度

目的 探讨1.7％七氟醚(1.0 MAC)吸入诱导下瑞芬太尼抑制喉罩插入反应的半数有效血浆靶控浓度(Cp50).方法 择期乳腺纤维瘤手术患者,年龄22～59岁,ASA Ⅰ或Ⅱ级.初始七氟醚吸入浓度为8％,氧流量4L/min,待患者意识消失后调整挥发罐浓度使七氟醚呼气末浓度为1.7％(1.0 MAC),维持3 min后靶控输注(TCI)瑞芬太尼,待计算效应室浓度等于血浆靶控浓度时行喉罩插入.瑞芬太尼血浆靶浓度按序贯法确定,起始浓度为6 ng/ml,相邻浓度比值为1.2.结果 最终有36例患者纳入本研究.TCI瑞芬太尼抑制喉罩插入反应的Cp50为1.91 ng/ml,95％可信区间(CI)为1.75～2.10 ng/ml.结论 七氟醚吸入诱导下TCI瑞芬太尼抑制喉罩插入反应的Cp50为1.91 ng/ml,95％CI为1.75～2.10 ng/ml.     

丙泊酚复合麻醉时神经外科手术患者雷米芬太尼的量效关系

目的 探讨丙泊酚复合麻醉时神经外科手术患者雷米芬太尼的量效关系.方法 择期额颞部开颅手术患者15例,先行靶控输注(TCI)阿泊酚,设定效应室靶浓度为3 μg/ml,维持PErCO2为35～45 mmHg,待达到丙泊酚靶浓度后开始TCI雷米芬太尼,设定效应室靶浓度分别为2、3、4、5、6、7、8ng/ml,雷米芬太尼达不同效应事浓度时给予50 mA、50 Hz、5 s强直电刺激,记录电刺激前后BP、HR及脑电双频指数(BIS)的变化.结果 随着雷米芬太尼效应室浓度的增加,BP逐渐降低,HR逐渐减慢(P<0.05或P<0.01);强直电刺激后BP升高幅度、HR加快幅度也逐渐降低(P<0.05或P<0.01).雷米芬太尼效应室浓度达(5.13±0.92)ng/ml时,强直电刺激后MAP升高幅度<5%,95%可信区间为3.33～6.93 ng/ml.与基础值比较,随着雷米芬太尼的效应室浓度逐渐增加,BIS逐渐降低(P<0.01),电刺激前后BIS无明显变化.结论 随雷米芬太尼效应室浓度的增加,镇痛强度逐渐增强,电刺激-循环反应逐渐减弱;雷米芬太尼效应室浓度大于(5.13±0.92)ng/ml时,95%可信区间为3.33～6.93ng/rnl,50 mA强直电刺激-循环反应变化小再明显.     

不同剂量右美托咪啶对七氟醚抑制切皮诱发患者体动反应肺泡气最低有效浓度的影响

目的 探讨不同剂量右美托咪啶对七氟醚抑制切皮诱发患者体动反应肺泡气最低有效浓度(MAC)的影响.方法 择期拟在全麻下行下腹部手术患者,性别不限,年龄18～64岁,体重指数21 ～ 27 kg/m2,ASA分级Ⅰ或Ⅱ级.采用随机数字表法,将其随机分为4组:对照组(C组)和不同剂量右美托咪啶组(D1组、D2组和D3组).麻醉诱导前静脉输注右美托咪啶(生理盐水稀释至15 ml)0.2μg/kg(D1组)、0.4 μg/kg(D2组)、0.6μg/kg(D3组)或生理盐水15 ml(C组),30 min内输注完毕.4组均采用吸入七氟醚麻醉诱导,气管插管后行机械通气.采用序贯法确定麻醉维持期间呼气末七氟醚浓度.C组、D1组、D2组及D3组第1例患者呼气末七氟醚浓度分别设定为3.0％、3.0％、2.5％和2.0％,预定呼气末七氟醚浓度稳定15 min时进行切皮.评估患者切皮时体动反应,当发生体动反应时,上调一个浓度梯度,否则下调一个浓度梯度,相邻浓度比值为0.9,根据前一例患者是否发生体动反应确定下一例患者呼气末七氟醚浓度,直至每组出现第7个交叉点.以各交叉点呼气末七氟醚浓度的均数作为MAC值,并计算95％可信区间 (CI).结果 C组、D1组、D2组和D3组入选病例分别18、20、20、22例；C组、D1组、D2组和D3组七氟醚MAC值(95％CI)分别为2.5％(2.3％～2.8％)、1.5％(1.3％～1.7％)、1.3％(1.0％～1.6％)和1.1％(0.7％ ～ 1.5％).与C组比较,D1组～D3组七氟醚MAC值降低(P＜0.05)；与D1组比较,D2组和D3组七氟醚MAC值降低(P＜0.05)；D2组和D3组七氟醚MAC值差异无统计学意义(P＞0.05).结论 右美托咪啶0.2、0.4、0.6 μg/kg可明显降低七氟醚抑制手术患者切皮诱发体动反应的MAC值,且呈剂量依赖性.     

安氟醚阻断小儿交感反应的最低肺泡有效浓度

目的　测定两个不同年龄段的小儿安氟醚的最低肺泡有效浓度 ,即MACbar。方法　2 8例ASAⅠ～Ⅱ级择期行腹部手术的小儿 ,分为三组 :大于 1岁单用安氟醚组 ;大于 1岁加用芬太尼组 ;6～ 12月龄单用安氟醚组。用丙泊酚 3mg/kg、维库溴铵 0 15mg/kg诱导 ,吸入安氟醚和氧气维持麻醉。大于 1岁加用芬太尼组 ,在切皮前 5min ,静脉加芬太尼 3μg/kg。各组MACbar的测定采用“上下法” ,起始浓度为 1MAC。前一病人的反应若为阳性 ,后一病人的肺泡浓度则上调0 3MAC ;若为阴性则下降 0 3MAC。切皮后 5min内的血压或心率的升高≥切皮前即刻的 15 %为交感神经反应阳性 ,<15 %则为阴性。结果　大于 1岁小儿安氟醚的MACbar值为 (3 2± 0 5 ) % ,95 %可信区间为 (2 8～ 3 6 ) % ;6～ 12月龄者为 (3 4± 0 5 ) % ,95 %可信区间为 (3 0～ 3 8) % ;3μg/kg芬太尼可以使大于 1岁小儿安氟醚的MACbar值降为 (2 2± 0 4 ) % ,95 %可信区间为 (1 8～2 5 ) %。结论　大于 6个月的小儿 ,安氟醚的肺泡浓度维持 3 3%左右 ,即约 1 5MAC ,可以阻断5 0 %的病人在切皮时的交感神经反应 ;3μg/kg芬太尼可以使其降低到约 1MAC。     

依托咪酯乳剂诱导时雷米芬太尼抑制气管插管反应的效应室靶浓度

目的 测定依托咪酯乳剂诱导时雷米芬太尼抑制气管插管反应的效应室靶浓度(EC50和EC95).方法 选择23例ASAⅠ或Ⅱ级全麻择期手术患者靶控输注(TCI)雷米芬太尼,血浆浓度与效应室浓度达到平衡后静脉注射依托咪酯乳剂0.3 mg/kg,患者意识消失后静脉注射琥珀胆碱行气管插管.气管插管后2 min内最高的SBP和/或HR高出基础值15%为气管插管反应阳性.雷米芬太尼靶浓度按改良序贯法增加或减少0.5 ng/ml.用概率单位回归分析法计算出雷米芬太尼抑制气管插管反应的EC50、EC95及相应的95%可信区间(CI).结果 雷米芬太尼抑制气管插管反应的EC50为3.06 ng/ml,95%CI为2.56～3.47 ng/ml;相应的EC95为3.85 ng/ml,95%CI为3.45～6.64ng/ml.结论 复合依托咪酯0.3 mg/kg诱导时雷米芬太尼抑制气管插管反应的EC50和EC95分别为3.06 ng/ml和3.85 ng/ml.     

异氟醚静脉复合麻醉在心脏手术中的应用

用异氟醚静脉复合麻醉于心内直视手术20例。先静注γ-OH40mg/kg或安定0.1mg/kg,吸入0.2-2％异氟醚(半紧闭法),再静注琥珀胆碱1mg/kg和芬太尼2μg/kg,气管插管。继用0.4-1.0％异氟醚(紧闭法)维持麻醉。切皮前再静注首次剂量1/2芬太尼。用Normac测定呼气末异氟醚浓度,Nccom3测量心排血量等循环功能指标。结果表明,麻醉各阶段平均呼气末浓度为0.5MAC,最高0.84MAC,最低0.38MAC。异氟醚对循环功能抑制小,复合静脉麻醉可维持适当麻醉深度,避免异氟醚增侠心率相降低平均动脉压的缺点,具有一定优越性。     

靶控输注丙泊酚和雷米芬太尼在意识消失和对疼痛刺激反应时的相互关系

目的探讨靶控输注(TCI)丙泊酚和雷米芬太尼的相互关系及对脑电双频指数(BIS)的影响。方法全身麻醉患者100例,根据丙泊酚不同血浆靶浓度随机均分为五组:P1.5组,1.5μg/ml;P2组,2μg/ml;P2.5组,2.5μg/ml;P3组,3μg/ml;P3.5组,3.5μg/ml。待血浆浓度和效应室浓度达到平衡后TCI雷米芬太尼,以血浆浓度0ng/ml为起点,每30秒增加0.3ng/ml,直至患者意识消失及对疼痛刺激(50Hz,80mA,0.25ms强直刺激)无体动反应。记录患者在不同丙泊酚血药浓度下意识消失时和对疼痛刺激无反应时雷米芬太尼的血浆浓度(Cp)和效应室浓度(EC)。结果意识消失时雷米芬太尼Cp50从P1.5组至P3.5组分别为5.0、3.0、2.1、1.2、0ng/ml;疼痛刺激无反应时雷米芬太尼Cp50从P1.5组至P3.5组分别为5.4、4.3、3.9、3.5、3.0ng/ml;疼痛刺激无反应时与意识消失时BIS值的差异无统计学意义。结论BIS值变化与丙泊酚血药浓度呈反比关系,雷米芬太尼对BIS值影响不大。BIS值50～60可以作为丙泊酚和雷米芬太尼静脉复合麻醉时监测意识消失的良好指标。     

瑞芬太尼预先给药对地氟醚诱发患者交感神经兴奋作用的影响

目的 探讨瑞芬太尼预先给药对地氟醚诱发患者交感神经兴奋作用的影响.方法 择期行耳鼻喉手术患者45例,年龄18～46岁,体重40～75 kg,性别不限,ASA Ⅰ级,随机分为3组:C组、R1组和R2组,每组15例.3组均静脉注射异丙酚1.5 mg/kg,R,组和R2组靶控输注瑞芬太尼,血浆靶浓度分别为1、2 ng/ml,C组给予生理盐水.待患者意识消失(呼之不应)后,吸人地氟醚,调节地氟醚吸入浓度,地氟醚呼气末浓度逐渐达0.5 MAC(T1)、1.0 MAC(T2)、1.5 MAC(T3),每一浓度维挣5min,同时监测心率变异性,分析出低频(LF)、高频(HF)及低频/高频比值(LF/HF),记录心率(HR)和平均动脉压(MAP).结果 与C组及R1组比较,R2组T2,3时HR、MAP及LF/HF降低,HF升高(P＜0.05).结论 瑞芬太尼血浆靶浓度2 ng/ml预先给药可抑制地氟醚诱发患者交感神经兴奋作用.     

Anesthetic Potency of Remifentanil in Dogs

Background: Remifentanil is an opioid that is rapidly inactivated by esterases in blood and tissues. This study examined the anesthetic potency and efficacy of remifentanil in terms of its reduction of enflurane minimum alveolar concentration (MAC) in dogs.

Methods: Twenty-five dogs were anesthetized with enflurane. One group received incremental infusion rates of remifentanil from 0.055 to 5.5 micro gram *symbol* kg sup -1 *symbol* min sup -1. A second group received constant rate infusions of remifentanil of 1.0 micro gram *symbol* kg sup -1 *symbol* min sup -1 for 6-8 h. Enflurane MAC was measured before, hourly during remifentanil infusion, and at the end of the experiment after naloxone administration. A third group received alternating infusions of 0.5 and 1.0 micro gram *symbol* kg sup -1 *symbol* min sup -1 with MAC determinations made 30 min after each change in the infusion rate. Heart rate, mean arterial pressure, and remifentanil blood concentrations were measured during MAC determinations.

Results: Enflurane MAC was reduced up to a maximum of 63.0+/- 10.4% (mean+/-SD) in a dose-dependent manner by remifentanil infusion. The dose producing a 50% reduction in the enflurane MAC was calculated as 0.72 micro gram *symbol* kg sup -1 *symbol* min sup -1 and the corresponding blood concentration was calculated as 9.2 ng/ml. Enflurane MAC reduction remained stable during continuous, constant rate infusions for periods of 6-8 h without any signs of tolerance. Recovery of enflurane MAC to baseline occurred in 30 min (earliest measurement) after stopping the remifentanil infusion.     

Reduction of Isoflurane Minimal Alveolar Concentration by Remifentanil

Background: Remifentanil is a new micro-specific opioid receptor agonist currently under investigation. The interaction between opioids and volatile anesthetics is complex. Defining this interaction provides a basis for more rational dosing schemes when such combinations are used for anesthesia and allows the anesthetic potency of remifentanil relative to other opioids to be determined.

Methods: Two centers enrolled a total of 220 patients. Patients were randomized to receive a target concentration of remifentanil via a computer-assisted continuous infusion device of either 0.0, 0.5, 1.0, 1.5, 2.0, 4.0, 8.0, 16.0, and 32.0 ng/ml initiated before the administration of isoflurane. Patients were also stratified by age groups 18-30, 31-55, and 56-65 yr. After induction of anesthesia with isoflurane the initial patient in each dose group was assigned an age-adjusted isoflurane concentration. The isoflurane concentration for each subsequent patient was adjusted according to the up/down technique until a minimum of 12 patients were enrolled in each group. Arterial blood samples for remifentanil whole blood concentrations were obtained. The patient was observed for purposeful movement for up to 1 min after skin incision. The minimum alveolar concentration (MAC) of isoflurane (0 ng/ml remifentanil group) and MAC reduction of isoflurane by remifentanil were determined.

Results: The MAC of isoflurane alone was 1.3%. Remifentanil caused an exponential reduction in the MAC of isoflurane with 1.37 ng/ml remifentanil resulting in a 50% MAC reduction, 4 ng/ml remifentanil a 77% reduction and 32 ng/ml a 91% reduction of isoflurane MAC.     

Sevoflurane--nitrous oxide anaesthesia supplemented with remifentanil: effect on recovery and cognitive function

The aim of this study was to compare recovery and psychomotor performance after maintenance of anaesthesia with sevoflurane or sevoflurane supplemented with remifentanil. Sixty-six per cent nitrous oxide was used in all patients. Twenty patients each were randomly allocated to maintenance of anaesthesia with sevoflurane only in concentrations necessary to maintain adequate anaesthesia or with 1.5, 1.0 or 0.5 MAC (end-tidal) of sevoflurane supplemented with remifentanil. The median dosage of remifentanil required in the last three groups was 0.21, 0.25 and 0.34 microg x kg(-1) x min(-1), respectively (p < 0.05). The median times to eye opening were 10.3, 12.7, 11.0 and 6.5 min in the four groups (p < 0.05 between the 0.5 MAC and the other groups) and for orientation 12.1, 14.9, 12.3 and 8.3 min, respectively (p < 0.05 between 0.5 and 1.5 MAC groups). There was no significant difference in the mini-mental state assessment scores or the actual discharge times from the recovery ward among the groups. Significantly greater numbers of patients could perform the critical flicker fusion test at 15 min in the group receiving the lowest concentration of sevoflurane and the highest dosage of remifentanil (p < 0.05). Patients in this group also showed the highest incidence of chest wall rigidity (p < 0.003). We conclude that, while the use of remifentanil with lower concentrations of sevoflurane facilitates early recovery, it does not influence discharge time from recovery ward and may be associated with side-effects such as chest wall rigidity.     

Plasma cortisol in experimental anesthesia with halothane, enflurane, isoflurane and nitrous oxide

The influence of anesthesia on plasma cortisol has most often been studied in connection with routine operations. To investigate the specific effects of modern inhalation anesthetics more accurately, we examined the specific effects of four inhalation anesthetics on human plasma cortisol during volunteer studies on the influence of anesthetics on the electroencephalogramm. METHODS. A group of 17 (10 m, 7 f) young healthy volunteers who had not received any premedication and were not intubated were studied after informed consent had been obtained. In the first series of experiments the concentration of halothane, enflurane, isoflurane or N2O was increased to MAC (minimal alveolar concentration) 0.5 for a 15-min steady-state period. Blood samples were taken 5 min prior to induction (I), 35 min after induction, on steady-state MAC 0.5 (II), and 15 (III) and 35 (IV) min after the end of anesthesia. In a second series, with 5 subjects, the concentration of halothane, enflurane or isoflurane was first increased to a steady state of MAC 1.0. After reduction to MAC 0.5 steady-state, anesthesia was supplemented with 53% N2O to give a steady state of MAC 1.0 again. Blood samples were taken 5 min prior to induction (I), after the attainment of steady-state MAC 1.0 (II), 35 min later at MAC 0.5 (III), 40 min later at MAC 1.0 with volatile anesthetic/N2O (IV), and 15 (V) and 35 (VI) min after the end of anesthesia. RESULTS. MAC 0.5 N2O produced a marked rise in mean plasma cortisol, from 64.2 micrograms/l to 164.5 micrograms/l.(ABSTRACT TRUNCATED AT 250 WORDS)     

不同血浆靶浓度瑞芬太尼对患儿吸入七氟烷诱导气管插管最低肺泡有效浓度的影响

目的 评价不同血浆靶浓度瑞芬太尼对患儿吸入七氟烷诱导气管插管最低肺泡有效浓度(MAC)的影响.方法 择期全麻患儿126例,年龄3～8岁,ASAⅠ或Ⅱ级,随机分为4组,对照组(C组,n=30);R1组(n=30)、R2组(n=30)和R3组(n=36)瑞芬太尼血浆靶浓度分别为1、2、3 ng/ml.均吸入5%七氟烷行麻醉诱导,睫毛反射消失后鼻腔置入导管连接气体分析仪,建立静脉通路,注射阿托品0.01 mg/kg,R1-3 组靶控输注瑞芬太尼.C组注射阿托品、R1-3组瑞芬太尼血浆浓度与效应室浓度达平衡后,采用改良序贯法进行试验,初始呼气末七氟烷浓度均为3.0%,相邻浓度比值为1.2,七氟烷呼气末浓度达到预定值并维持10 min后行气管插管.气管插管条件满意的标准:气管插管条件评分为6分.计算每组七氟烷MAC,并观察不良反应的发生情况.结果 C组、R1-3组患儿吸入七氟烷诱导气管插管的MAC分别为5%、3%、2%、1%,依次降低(P<0.01);所有患儿均无心动过缓、低血压等发生,R2组3例、R3组8例患儿因下颌松弛度差致喉镜无法置人或声门关闭,静脉注射罗库溴铵完成气管插管.结论 瑞芬太尼1 ng/ml可降低患儿吸入七氟烷诱导气管插管的最低肺泡有效浓度,且不良反应少.     

末梢灌注指数监测地氟醚诱发患者交感神经兴奋的评价

目的 评价末梢灌注指数(TPI)监测地氟醚诱发的患者交感神经兴奋作用.方法 择期全麻患者48例,年龄25～60岁,ASA Ⅰ或Ⅱ级,随机分为3组(n=16):七氟醚组(Ⅰ组)、地氟醚组(Ⅱ组)和地氟醚+异丙酚组(Ⅲ组).气管插管后Ⅰ组和Ⅱ组地氟醚或七氟醚呼气末浓度依次快速达到0.5 MAC、1.0 MAC和1.5 MAC,并在每个水平维持5 min.Ⅲ组在气管插管后靶控输注异丙酚.血浆靶浓度至1μg/ml,地氟醚呼气末浓度依次快速达到0.5 MAC、1.0 MAC,并在每个水平维持5 min.分别在给予咪达唑仑后5 min(T0)、麻醉诱导后3 min(T1)、插管后即刻(T2)、呼气末浓度达到0.5 MAC(T3)、0.5 MAC后5 min(T4)、1.0 MAC(T5)、1.0MAC后5min(T6)、1.5MAC(T7)、1.5MAC后5min(T8)时记录心率(HR)、平均动脉压(MAP)、TPI、脑电双频谱指数,并在T0、T1、T2、T5、T7时测定血浆肾素活性和血管紧张素Ⅱ水平.结果 与T4时比较,Ⅱ组T5时,IPI降低(P<0.05);与T7时比较,Ⅱ组T4～6、T8时HR、MAP降低,T3～6、T8时TPI降低(P<0.05);与Ⅰ组比较,Ⅱ组T7时HR、MAP升高,TPI降低(P<0.05);Ⅱ组T5和T7时TPI出现变化最大值的时间短于HR、MAP;ATPI与△HR、AMAP呈负相关(r=-0.593,P<0.05;r=-0.591,P<0.05);与Ⅰ组比较,Ⅱ组血浆肾素活性和AT-Ⅱ浓度升高(P<0.05).结论 TPI可灵敏地反映地氟醚诱发的患者交感神经兴奋.     

Effects of two target-controlled concentrations (1 and 3 ng/ml) of remifentanil on MAC(BAR) of sevoflurane

BACKGROUND: The aim of this prospective, randomized, double-blind study was to determine the effects of two different target-controlled concentrations of remifentanil (1 and 3 ng/ml) on the sevoflurane requirement for blunting sympathetic responses after surgical incision (MACBAR). METHODS: Seventy-four patients aged 20-50 yr, with American Society of Anesthesiologists physical status I, were anesthetized with propofol, cisatracurium, and sevoflurane with a mixture of 60% nitrous oxide in oxygen. Then, patients were randomly allocated to receive no remifentanil infusion (n = 27) or a target-controlled plasma concentration of 1 ng/ml (n = 27) or 3 ng/ml remifentanil (n = 20). Sympathetic responses to surgical incision (presence or absence of an increase in either heart rate or mean arterial blood pressure of 15% or more above the mean of the values measured during the 2 min before skin incision) were determined after a 20-min period of stable end-tidal sevoflurane and target-controlled remifentanil concentrations. Predetermined end-tidal sevoflurane concentrations and the MACBAR for each group were determined using an up-and-down sequential-allocation technique. RESULTS: The MACBAR of sevoflurane was higher in the group receiving no remifentanil (2.8% [95% confidence interval: 2.5-3.0%]) as compared with patients of the groups receiving 1 ng/ml (1.1% [0.9-1.3%]; P = 0.012) and 3 ng/ml remifentanil (0.2% [0.1-0.3%]; P = 0.006). When considering a minimum anesthetic concentration (MAC) value in this age population and the contribution of 60% nitrous oxide (0.55 MAC), the combined MACBAR values, expressed as multiples of the MAC, were 1.95 MAC, 1.1 MAC, and 0.68 MAC, in the three groups, respectively. CONCLUSION: A target-controlled concentration of 1 ng/ml remifentanil results in a 60% decrease in the MACBAR of sevoflurane combined with 60% nitrous oxide. Increasing the target concentration of remifentanil to 3 ng/ml produces a further 30% decrease in the MACBAR values of sevoflurane.     

Effects of Two Target-controlled Concentrations (1 and 3 ng/ml) of Remifentanil on MACBAR of Sevoflurane

Background: The aim of this prospective, randomized, double-blind study was to determine the effects of two different target-controlled concentrations of remifentanil (1 and 3 ng/ml) on the sevoflurane requirement for blunting sympathetic responses after surgical incision (MACBAR).

Methods: Seventy-four patients aged 20-50 yr, with American Society of Anesthesiologists physical status I, were anesthetized with propofol, cisatracurium, and sevoflurane with a mixture of 60% nitrous oxide in oxygen. Then, patients were randomly allocated to receive no remifentanil infusion (n = 27) or a target-controlled plasma concentration of 1 ng/ml (n = 27) or 3 ng/ml remifentanil (n = 20). Sympathetic responses to surgical incision (presence or absence of an increase in either heart rate or mean arterial blood pressure of 15% or more above the mean of the values measured during the 2 min before skin incision) were determined after a 20-min period of stable end-tidal sevoflurane and target-controlled remifentanil concentrations. Predetermined end-tidal sevoflurane concentrations and the MACBAR for each group were determined using an up-and-down sequential-allocation technique.

Results: The MACBAR of sevoflurane was higher in the group receiving no remifentanil (2.8% [95% confidence interval: 2.5-3.0%]) as compared with patients of the groups receiving 1 ng/ml (1.1% [0.9-1.3%]; P = 0.012) and 3 ng/ml remifentanil (0.2% [0.1-0.3%]; P = 0.006). When considering a minimum anesthetic concentration (MAC) value in this age population and the contribution of 60% nitrous oxide (0.55 MAC), the combined MACBAR values, expressed as multiples of the MAC, were 1.95 MAC, 1.1 MAC, and 0.68 MAC, in the three groups, respectively.     

Effects of remifentanil/propofol in comparison with isoflurane on dynamic cerebrovascular autoregulation in humans

BACKGROUND: This study investigates the effects of remifentanil and propofol in comparison to isoflurane on dynamic cerebrovascular autoregulation in humans. METHODS: In 16 awake patients dynamic cerebrovascular autoregulation was measured using transcranial Doppler sonography (TCD). Thereafter patients were intubated, ventilated with O2/air (FiO2=0.33) and randomly assigned to one of the following anesthetic protocols: group 1 (n=8): 0.5 microg x kg(-1) x min(-1) remifentanil combined with a propofol-target plasma concentration of 1.5 microg x ml(-1) group 2 (n=8): 1.8 % isoflurane (1.5 MAC). Following 20 min of equilibration the autoregulatory challenge was repeated. Arterial blood gases and body temperature were maintained constant over time. Statistics: Mann-Whitney U-test and Wilcoxon signed-rank test. RESULTS: Dynamic autoregulation was intact in all patients prior to induction of anesthesia expressed by an autoregulatory index (ARI) of 5.4+/-1.21 (mean+/-SD, group 1) and 5.9+/-0.98 (mean+/-SD, group 2). With remifentanil/propofol anesthesia dynamic autoregulation was similar to the awake state (group 1: ARI=4.9+/-0.88). In contrast, autoregulatory response was delayed with 1.5 MAC isoflurane (group 2, ARI=2.1+/-0.92) (P<0.05). CONCLUSION: These data show that dynamic cerebrovascular autoregulation is maintained with remifentanil-based total intravenous anesthesia. This is consistent with the view that narcotics (and hypnotics) do not alter the physiologic cerebrovascular responses to changes in MAP. In contrast, 1.5 MAC isoflurane delays cerebrovascular autoregulation compared to the awake state.