国产顺苯磺酸阿曲库铵在小儿麻醉中的应用

目的观察不同剂量国产顺苯磺酸阿曲库铵用于小儿的药效学。方法45例2~12岁患儿随机均分为三个顺苯磺酸阿曲库铵剂量组:2ED95组(C2组)、3ED95组(C3组)和4ED95组(C4组)。采用TOF-Guard肌松监测仪测定拇内收肌诱发颤搐反应变化,观察气管插管条件及顺苯磺酸阿曲库铵的药效学。结果三组均能完成气管插管。C3组和C4组插管条件评分均为5分;C2组中仅33.3%的患者插管条件评分>5分。随剂量增加,顺苯磺酸阿曲库铵阻滞起效时间相应缩短,肌松作用时间随剂量增加而延长,肌松恢复指数组间差异无统计学意义。所有患儿均无过敏反应发生。结论顺苯磺酸阿曲库铵随剂量的增加起效时间缩短,肌松作用时间延长。3ED95国产顺苯磺酸阿曲库铵剂量作为小儿气管插管较为合适。     

恶性肿瘤对顺阿曲库铵肌松效应的影响

目的 探讨恶性肿瘤对顺阿曲库铵肌松效应的影响.方法 选择头颈部肿瘤患者60例,ASA分级Ⅰ或Ⅱ级,年龄18～64岁,分为4组(n=15),良性肿瘤组(B组,3×ED95);45例恶性肿瘤患者按顺阿曲库铵使用剂量分为C1组(2×ED95)、C2组(3×ED95)和C3组(4 × E95).采用TOF-Watch SX型加速度肌松监测仪对尺神经行单次颤搐刺激,监测拇内收肌颤搐情况.麻醉诱导:靶控输注异丙酚(血浆靶浓度3μg//ml)和瑞芬太尼(效应室靶浓度3 ng/ml),患者意识消失后开启加速度肌松监测仪.B组静脉注射顺阿曲库铵0.15 mg/kg行气管插管.C1组、C2组和C3组分别静脉注射顺阿曲库铵0.10、0.15和0.20mg/kg行气管插管.记录顺阿曲库铵起效时间,临床作用时间、T/Tc恢复至75%的时间及其恢复指数.结果 与B组比较,C2组顺阿曲库铵临床作用时间、T/Tc恢复至75%的时间及恢复指数延长(P＜0.05),起效时间差异无统计学意义(P＞0.05).与C1组比较,C2组和C3组顺阿曲库铵起效时间缩短,临床作用时间、T/Tc恢复至75%的时间延长(P＜0.05),恢复指数差异无统计学意义(P＞0.05).与C2组比较,C3组顺阿曲库铵起效时间缩短,临床作用时间、T/Tc恢复至75%时间延长(P＜0.05),恢复指数差异无统计学意义(P＞0.05).结论 恶性肿瘤患者应用顺阿曲库铵肌松效应的维持和恢复时间延长.     

顺苯磺酸阿曲库铵临床有效剂量测定

目的 测定1倍95％有效量(ED95)顺阿曲库铵对神经肌肉接头的阻滞时程和恢复过程.方法 择期全麻手术患者30例,随机均分为Ⅰ、Ⅱ和Ⅲ组.Ⅰ组:顺苯磺阿曲库铵(批号:1067,葛兰素史克公司)稀释到10 ml,1 mg/ml;Ⅱ组:将顺苯磺酸阿曲库铵(批号:11111213,恒瑞医药股份有限公司)溶解到10 ml,认为顺苯磺阿曲库铵浓度为1 mg/ml;Ⅲ组:将顺苯磺酸阿曲库铵(同Ⅱ组)溶解到7.5 ml,假设顺阿曲库铵浓度为1 mg/ml.丙泊酚和舒芬太尼麻醉诱导后分别静脉注射1倍ED95顺阿曲库铵.用TOF Watch SX加速度仪对近腕尺神经行TOF透皮刺激,观察与记录给予肌松药的起效时间、第一次反应(T1)最大阻滞程度(Tmax)和临床有效时间.结果 三组起效时间差异无统计学意义.Ⅰ组Tmax和临床有效时间与Ⅲ组比较差异无统计学意义;Ⅱ组Tmax和临床有效时间明显低于Ⅰ组和Ⅲ组(P＜0.01或P＜0.05).结论 恒瑞医药股份有限公司的顺苯磺酸阿曲库铵每瓶含顺阿曲库铵约7.5 mg.使用时溶解成7.5 ml,能使顺阿曲库铵浓度达到1 mg/ml.     

小儿不同剂量顺式阿曲库铵的肌松作用

目的通过观察小儿不同剂量顺式阿曲库铵的肌松作用,评价是否存在封顶效应,探讨小儿合适的麻醉诱导剂量。方法45例择期手术的息儿,年龄15～50月,ASAⅠ或Ⅱ级,随机分为3组(n=15):顺式阿曲库铵0.1 mg/kg组(A组)、顺式阿曲库铵0.15 mg/kg组(B组)、顺式阿曲库铵0.2 mg/kg(C组)。采用TOF-Guard肌松监测仪对尺神经行连续四个成串(TOF)刺激,监测拇内收肌肌颤搐变化;静脉注射异丙酚2 mg/kg、芬太尼2μg/kg及相应剂量顺式阿曲库铵麻醉诱导,吸入O2-N2O和静脉持续输注异丙酚维持麻醉;评价气臂插管条件评估分级,监测诱导期间血液动力学变化,记录起效时间(肌松药注毕至T1达最大抑制的时间)、临床肌松维持时间(肌松药注毕至T1恢复5%的时间)、临床肌松有效作用时间(T1从最大抑制至恢复25%的时间)、恢复指数(T1恢复从25%至75%的时间)、体内肌松作用时间(肌松药注毕至T1恢复95%的时间)。结果3组气管插管条件评估分级比较差异无统计学意义;三组T1达最大抑制时心率、平均动脉压组间和组内比较差异均无统计学意义。与A组相比,B组、C组起效时间较短,临床肌松维持时间、临床肌松有效作用时间、体内肌松作用时间较长(P<0.01);三组恢复指数差异无统计学意义。与B组相比,C组起效时间差异无统计学意义,但临床肌松维持时间、临床肌松有效作用时间、体内肌松作用时间较长(P<0.05或0.01)。结论小儿芬太尼复合异丙酚时,顺式阿曲库铵0.15 mg/kg(3倍ED95)是麻醉诱导的适宜剂量。     

老年患者顺苯磺酸阿曲库铵的药效动力学

目的 研究顺苯磺酸阿曲库铵肌松效应的年龄差异.方法 196例患者按年龄分为四组:Ⅰ组53例,32～59岁;Ⅱ组54例,60～69岁;Ⅲ组52例,70～89岁;Ⅳ组37例,90～97岁.四组患者均于全麻诱导时静注顺苯磺酸阿曲库铵0.15 mg/kg.并进行TOF肌松监测.术中持续泵注顺苯磺酸阿曲库铵,维持T结果10%～20%至术中结束.记录顺苯磺酸阿曲库铵药效动力学参数.结果 Ⅳ组肌松起效时间短于其他三组(P<0.01);Ⅰ、Ⅱ组首次给药后T125%恢复时间显著快于Ⅲ、Ⅳ组(P<0.01);顺苯磺酸阿曲库铵用量随年龄增加而减少(P<0.01).结论 随年龄的增长,顺苯磺酸阿曲库铵起效时间缩短,肌松持续时间延长,维持用量减少.     

米库氯铵与顺苯磺酸阿曲库铵在婴幼儿唇腭裂手术中的应用比较

目的观察和比较米库氯铵和顺苯磺酸阿曲库铵用于婴幼儿唇腭裂手术中的肌松效应和安全性。方法 2012年9月至2013年9月择期行唇腭裂手术治疗的患儿60例,年龄6个月至3岁,随机分为两组,每组30例。两组均给予咪达唑仑0.1mg/kg、丙泊酚2mg/kg、瑞芬太尼1μg/kg及米库氯铵0.2mg/kg(M组)或顺苯磺酸阿曲库铵0.15mg/kg(C组)行麻醉诱导后气管插管。采用TOF-Guard加速度肌松监测仪连续监测尺神经四个成串刺激(TOF)。观察并记录肌松起效时间、临床作用时间和恢复指数,进行插管评级并观察不良反应情况。结果两组的插管条件评级差异无统计学意义。M组肌松起效时间、肌松临床作用时间以及恢复指数明显短于C组(P0.05);M组不良反应发生率明显低于C组(P0.05)。结论米库氯铵用于婴幼儿唇腭裂手术时起效快、肌松效应时间短,恢复较快。     

罗库溴铵和阿曲库铵联合应用的肌松效应分析

目的探讨罗库溴铵和阿曲库铵联合应用时的肌松效应。方法择期全麻手术女性成年患者147例,丙泊酚和舒芬太尼静脉诱导,输注丙泊酚维持麻醉。面罩辅助或控制呼吸,用加速度仪以连续4次刺激(TOF)方式透皮刺激腕部尺神经,获取肌松药作用起效时间和T1最大抑制程度(Tmax)。按观测项目将患者均分成四组。结果阿曲溴铵ED95为(220.8±3.6)μg/kg,罗库溴铵ED95为(286.3±3.1)μg/kg。0.5×ED95的罗库溴铵与阿曲库铵联合使用,肌松效应达到T1抑制93%~97%时,阿曲库铵的剂量为63.6μg/kg。罗库溴铵0.5×ED95与阿曲库铵63.6μg/kg联合使用,Tmax为(95.3±0.9)%,变异系数1.0%。Ⅳ组中三个亚组的Tmax基本相同,合用组作用起效时间比阿曲库铵组快(P<0.01)。给予肌松药前和注药后5min内,MAP和HR的波动幅度均小于5%。结论罗库溴铵与阿曲库铵合用呈协同作用。当罗库溴铵剂量为0.5×ED95时,为获得T1抑制95%的肌松效应,阿曲库铵的合理用量为63.6μg/kg,比阿曲库铵的ED95减少71.2%。     

不同性别患者预注顺阿曲库铵加快起效的半数有效剂量

目的 探讨不同性别患者预注顺阿曲库铵加快起效的半数有效剂量(ED50).方法 择期拟在全身麻醉下行腹部手术的患者90例,年龄18～55岁,分为2组(n=45):男性组(M组)和女性组(F组).采用TOF-Watch SX型加速度肌松监测仪对尺神经行单次颤搐刺激,监测拇内收肌肌颤搐情况.静脉注射咪达唑仑0.04 mg/kg、芬太尼1 μg/kg,患者意识消失后开启加速度肌松监测仪,静脉注射顺阿曲库铵预注剂量,3 min后静脉注射芬太尼5 μg/kg、异丙酚2 mg/kg,静脉注射预注量后4 min,静脉注射顺阿曲库铵剩余插管剂量(3×ED95即0.15 mg/kg减去预注量),当单刺激颤搐值与对照值的比值下降至10%,行气管插管.静脉输注异丙酚、瑞芬太尼,吸入异氟烷维持麻醉.预注量根据序贯法确定,预注量从5μg/kg(10%ED95)开始,各相邻剂量比值为1.2.记录给予预注量后4min时单刺激颤搐值与对照值的比值、90%起效时间、起效时间、最大阻滞程度、临床作用时间.计算预注顺阿曲库铵加快起效的ED50及其95%可信区间(CI).结果 M组90%起效时间长于F组(P＜0.05),其余肌松效应指标两组比较差异无统计学意义(P＞0.05).预注顺阿曲库铵加快起效的ED50:男性为21.36μg/kg,95%CI为20.52～22.23μg/kg;女性为14.53 μg/kg,95%CI为13.77～15.33μg/kg,男性高于女性(P＜0.05).结论 预注顺阿曲库铵加快起效的ED50:男性为21.36μg/kg,女性为14.53 μg/kg,男性高于女性.     

阿曲库铵与哌库溴铵在预注法中的复合应用

目的 观察阿曲库铵和哌库溴铵在预注法中的复合应用。方法 选择平衡麻醉下择期手术病人70例。研究分两部分：第一部分，将30例病人随机均分为阿曲库铵组和哌库溴铵组，采用累计给药法建立两药量一效关系曲线，计算ED50和ED95；第二部分，根据两药ED95将另40例病人随机均分为单纯阿曲库铵预注组和复合哌库溴铵预注组。观察预注期间肌颤搐抑制值、起效时间和临床作用时间。结果 阿曲库铵ED50和ED95分别为117．5μg／kg和272．8μg／kg，哌库溴铵ED50和ED95分别为23．7μg／kg和42．6μg／kg；复合哌库溴铵预注组起效快于单纯阿曲库铵预注组；复合哌库溴铵预注组临床作用时间长于单纯阿曲库铵预注组。结论 在预注法中采用化学结构不同的肌松药可进一步加快起效，延长临床作用时间。     

国人顺式阿曲库铵的剂量反应测定

目的　采用经典的单次注射法建立顺式阿曲库铵的剂量 -反应曲线 ,了解该肌松药应用于国人的量效关系 ,并确定其 ED50 、ED75、ED90 和 ED95值 ,为临床研究和应用提供参考。方法　 ASA ～ 级择期手术患者 2 4例 ,随机分为 4组。咪唑安定、依托咪酯、芬太尼麻醉。 4组病人分别单次静注顺式阿曲库铵 0 .0 2、0 .0 3、0 .0 4和 0 .0 5 m g/ kg,观察拇指内收肌四个成串刺激 ( TOF)第一次反应 ( T1 )最大抑制的百分率并进行概率单位转换。将顺式阿曲库铵的首次剂量进行对数转换 ,用直线回归方法建立顺式阿曲库铵的剂量 -反应曲线 ,同时记录起效时间。结果　顺式阿曲库铵的 ED50 、ED75、ED90和 ED95的值分别为 :0 .0 3、0 .0 3 9、0 .0 4 9和 0 .0 5 6mg/ kg。顺式阿曲库铵起效时间在四个剂量组之间无显著差异 ( P>0 .0 5 )。结论　国外文献报道顺式阿曲库铵的 ED95值为 0 .0 4 7～ 0 .0 5 3 mg/ kg。本文得到的 ED95值为 0 .0 5 6m g/ kg,与国外文献的报道相拟     

Cisatracurium am M. orbicularis oculi Vergleich der neuromuskulären Wirkung von Cisatracurium und Atracurium am M. orbicularis oculi und M. adductor pollicis

OBJECTIVES: Muscle relaxants have different pharmacodynamic profiles in various muscles. Therefore, results obtained for one muscle cannot be extrapolated to other muscles. In the adductor pollicis muscle cisatracurium exerts a pharmacodynamic profile comparable to atracurium, despite the known difference in onset time. However, studies evaluating the neuromuscular effect of cisatracurium in different muscles are lacking. Accordingly, this study compares the pharmacodynamic profile of cisatracurium and atracurium in the orbicularis oculi muscle (OO) - which shows a neuromuscular course similar to the diaphragm and the laryngeal muscles - and the adductor pollicis muscle (AP). METHODS: Forty-five patients (ASA I-II), scheduled for elective spinal surgery were anaesthetized with propofol and fentanyl. Endotracheal intubation was performed without using a muscle relaxant. Neuromuscular transmission was monitored using acceleromyography in both muscles. Patients received 0.1 mg/kg (2x ED(95)) or 0.15 mg/kg (3x ED(95)) cisatracurium, or 0.5 mg/kg atracurium (2x ED(95)) at random. Onset and recovery times were measured according to the recommendation of the Copenhagen Consensus Conference. RESULTS: Onset time was significantly shorter in the OO than in the AP following 0.15 mg/kg cisatracurium and 0.5 mg/kg atracurium (P<0.05). No differences in onset time between the two muscles were found after 0.1 mg/kg cisatracurium. The recovery of T(1) to 10% of its control was completed sooner in the OO than in the AP in all three groups (P<0.05). CONCLUSIONS: Cisatracurium shows a dose-dependent shorter onset time in the OO than in the AP. This is consistent with the current view that the onset of non-depolarizing neuromuscular blockers is more rapid in the OO than in the AP. However, at least a dose of 3x ED(95) of cisatracurium was necessary to show a difference in onset time between both muscles. In contrast, atracurium is reported to lead to a significantly shorter onset of neuromuscular block in the OO following 2x the ED(95). The more rapid recovery of T(1) to 10% of its control in all three groups in the OO is due to the relative resistance of this muscle to muscle relaxants.     

Is muscle relaxant necessary for cardiac surgery?

The need for continuous and complete paralysis during the entire cardiac surgery has not yet been investigated and is still controversial. In a series of 87 patients undergoing cardiac surgery with normothermic cardiopulmonary bypass, we studied the delay of recovery, incidence of residual paralysis, unwanted patient movement, and difficult surgical conditions after a single dose of atracurium (0.5 mg/kg) or cisatracurium (0.15 mg/kg). Anesthesia was induced with etomidate and remifentanil followed by tracheal intubation. The delay to obtain a train-of-four ratio of >0.9 was longer with cisatracurium than with atracurium (86 +/- 18 versus 97 +/- 19 min). However, at the end of surgery, this ratio was >0.9 for all patients. The presence of unwanted patient movement, diaphragmatic contractions, and difficult surgical conditions were observed. Delay of extubation of the trachea was similar in both groups. We conclude that there is no need for continuous neuromuscular blockade during cardiac surgery. A single dose of either atracurium or cisatracurium is sufficient to provide efficient paralysis from the start of induction leading to quicker recovery from paralysis in fast-track cardiac surgery.     

Dose-response relationships for edrophonium and neostigmine antagonism of atracurium and cisatracurium- induced neuromuscular block

PURPOSE: To study the dose-response relationships for neostigmine and edrophonium during antagonism of neuromuscular block induced by atracurium and cisatracurium. METHODS: One hundred and twenty eight, ASA group 1 or 2 adults were given either 0.5 mg x kg(-1) atracurium or 0.1 mg x kg(-1) cisatracurium during fentanyl-thiopental-nitrous oxide-isoflurane anesthesia. The neuromuscular block was measured by an acceleration-responsive transducer. Responses were defined in terms of percent depression in the first twitch (T1) and train-of-four (TOF) response. When spontaneous recovery of first twitch height reached 10% of its initial control value, edrophonium (0.1, 0.2, 0.4, or 1 mg x kg(-1)) or neostigmine (0.005, 0.01, 0.02, or 0.05 mg x kg(-1)) was administered by random allocation. Neuromuscular function in another sixteen subjects was allowed to recover spontaneously. RESULTS: At five minutes, unlike edrophonium, neostigmine was equally effective against atracurium and cisatracurium with respect to T1 recovery. The neostigmine T1-ED50 was 10.3 +/- 1.06 (SEM) microg x kg(-1) after atracurium and 11.2 +/- 1.06) microg x kg(-1) after cisatracurium. The edrophonium ED50 was 157 +/- 1.07 microg x kg(-1) with atracurium and 47.4 +/- 1.07 microg x kg(-1) with cisatracurium, giving a neostigmine:edrophonium potency ratios of 15.2 +/- 1.7 and 4.2 +/- 0.41 (P < 0.001) for atracurium and cisatracurium, respectively. At 10 min neostigmine was 13 +/- 1.4 times as potent as edrophonium for achieving 50% TOF recovery after atracurium paralysis. After cisatracurium the potency ratio was 11.8 +/- 1.3 (NS). CONCLUSIONS: Although there were differences at five minutes, neostigmine:edrophonium potency ratios at 10 min, were similar in both relaxants studied.     

Comparison of the neuromuscular blocking effect of cisatracurium and atracurium on the larynx and the adductor pollicis

BACKGROUND: Cisatracurium unlike atracurium is devoid of histamine-induced cardiovascular effects and this alone would be the greatest advantage in replacing atracurium for the facilitation of tracheal intubation. On the other hand, 2 ED(95) doses of cisatracurium (100 micro g/kg) do not yield satisfactory intubating conditions such as those seen with equipotent doses of atracurium and therefore the recommended intubating dose of cisatracurium is 3 ED(95). To understand this discrepancy better, we evaluated the potency and onset of atracurium and cisatracurium directly at the larynx adductors in humans. METHODS: The study was conducted in 54 patients (ASA class I or II) undergoing peripheral surgery requiring general anesthesia. Cisatracurium 25-150 micro g/kg or atracurium 120-500 micro g/kg intravenous (i.v.) boluses doses were administered during anesthesia with propofol, nitrous oxide, oxygen and fentanyl. Neuromuscular block was measured by electromyography (single twitch stimulation every 10 s) at the larynx and the adductor pollicis. The dose-response effect measured at both muscles included maximum neuromuscular blockade achieved (Emax), the time to maximum depression of twitch height (onset) and time to spontaneous recovery of the twitch height to 25%, 75% and 90% (T25, T75, T90) of control value. RESULT: The onset at the larynx was of 196 +/- 28 s after the 100 micro g/kg cisatracurium dose compared with 140 +/- 14 s after the 500 micro g/kg atracurium dose (P < 0.05). Emax at the larynx was 92 +/- 1% and 98 +/- 1% after 100 micro g/kg cisatracurium and 500 micro g/kg atracurium, respectively (P < 0.05). The time to onset of maximum suppression Emax = 100 +/- 0% after a 150 micro g/kg cisatracurium dose was 148 +/- 29 s. At the larynx, the ED(50) was 25 micro g/kg for cisatracurium and 180 micro g/kg for atracurium and the ED(95) was 87 micro g/kg for cisatracurium compared with 400 micro g/kg for atracurium. CONCLUSION: The slow onset time at the laryngeal muscles after cisatracurium can be explained by the higher potency as compared with atracurium.     

七氟烷对顺式阿曲库铵和罗库溴铵肌松作用的影响

目的：比较七氟烷对顺式阿曲库铵和罗库溴铵肌松效应的影响。方法：择期手术患者240例,随机分为顺式阿曲库铵组（CIS120例）和罗库溴铵组（ROC120例）。两组患者再随机分为丙泊酚组（60例）和七氟烷组（60例）,均静脉注射咪达唑仑、芬太尼和丙泊酚行麻醉诱导,丙泊酚组靶控输注丙泊酚维持麻醉,设定血浆靶控浓度2～6μg/mL,输注丙泊酚5min后静脉注射顺式阿曲库铵0.15mg/kg或罗库溴铵0.6mg/kg;七氟烷组在呼气末七氟烷浓度稳定于1MAC5min后静脉注射顺式阿曲库铵0.15mg/kg或罗库溴铵0.6mg/kg。结果：CIS两组,起效时间差异无统计学意义（P〉0.05）;七氟烷组完全肌松时间、维持时间与丙泊酚组比较均显著延长（P〈0.01）。ROC两组,起效时间差异无统计学意义（P〉0.05）;七氟烷组完全肌松时间、维持时间与丙泊酚组比较均显著延长（P〈0.01）。结论：七氟烷对顺式阿曲库铵及罗库溴铵的肌松均有增效作用。     

Comparative Pharmacology of Cisatracurium (51W89), Atracurium, and Five Isomers in Cats

Background: Atracurium has four chiral centers and the marketed product is a mixture of ten optical and geometric isomers. Six of the isomers were prepared and evaluated for neuromuscular blocking activity and autonomic effects in anesthetized cats. This study reports the comparative pharmacology of the six isomers and atracurium that led to the selection of one isomer, cisatracurium (Nimbex, 51W89) for clinical development.

Methods: Purpose bred cats, anesthetized with alpha-chloralose (80 mg/kg) and pentobarbital sodium (7 mg/kg) administered intraperitoneally, were used in this study. Neuromuscular blocking effects were assessed from the effects on the tibialis anterior twitch evoked at 0.15 Hz. Inhibition of the autonomic nervous system was assessed from the effects on the nictitating membrane contraction, in response to preganglionic sympathetic nerve stimulation and the bradycardia/vasodepressor responses to vagal nerve stimulation. Cardiovascular effects and plasma histamine concentrations were determined after a bolus injection of cisatracurium or atracurium.

Results: Like atracurium, all six isomers produced dose-dependent neuromuscular block (NMB). The calculated ED95 NMB values varied approximately tenfold (43+/-2 micro gram/kg-488+/-56 micro gram/kg). The "R-series" isomers were more potent than the corresponding "S series" isomers. With the exception of the S,Trans-S', Trans isomer, the NMB effects, i.e., onset times (range 2.6+/-0.2 min to 4.7+/-0.3 min) and total durations (range 9.9+/- 1.4 min to 14+/-0.9 min), of the other five isomers were very similar to that of atracurium. The former isomer had a relatively short duration of action. The 25-75% recovery times after cisatracurium at 1x ED sub 95 (4.4+/-0.4 min), 4x ED95 (4.5+/-0.4 min), and continuous infusions lasting at least 60 min that maintained 95-99% NMB (4.8+/-0.4 min) indicated a noncumulative effect. The vagal ID50: NMB ED95 ratios for atracurium and the six isomers ranged from 2 to 27. The sympathetic ID25: NMB ED95 ranged from 2.7 to 60. Atracurium and all of the isomers, except cisatracurium, produced cardiovascular effects after intravenous bolus administration at large doses (700-4,800 micro gram/kg). In contrast to atracurium, there were no changes in plasma histamine concentrations associated with the administration of doses of cisatracurium equivalent to 60x the NMB ED95 (62+/-8 micro gram/kg).     

The effects of cisatracurium on morbidly obese women

There is conflicting evidence on the duration of action of atracurium in obese patients. Cisatracurium is one of the stereoisomers of atracurium. We investigated the neuromuscular effects of cisatracurium in morbidly obese patients. Twenty obese female patients (body mass index >40) were randomized in two groups. Group I (n = 10) received 0.2 mg/kg of cisatracurium on the basis of real body weight (RBW), whereas in Group II (n = 10) the dose was calculated on ideal body weight (IBW). In a control group of 10 normal weight female patients (body mass index 20-24), the dose of cisatracurium was based on RBW. Neuromuscular transmission was monitored using acceleromyography of the adductor pollicis, and anesthesia was induced and maintained with remifentanil and propofol. Onset time was comparable between Group I and the control group (132 s versus 135 s; P = ns). The duration 25% was longer in Group I than in the control group (74.6 min versus 59.1 min; P = 0.01) and in the control group compared with Group II (45.0 min; P = 0.016). In conclusion, the duration of action of cisatracurium was prolonged in morbidly obese patients when dosed according to RBW compared with a control group of normal weight patients. Duration was also prolonged in the control group patients compared with morbidly obese patients to whom the drug was administered on the basis of IBW.     

A comparison of the neuromuscular blocking effects and reversibility of cisatracurium and atracurium

The neuromuscular blocking effects and the reversibility of cisatracurium 0.1 or 0.15 mgkg⁻¹ were compared with those of atracurium 0.5 mgkg⁻¹ during anaesthesia with propofol, nitrous oxide and isoflurane. Neuromuscular block was monitored using train-of-four stimulation while recording the mechanomyographic response of the adductor pollicis muscle. The block was either allowed to recover spontaneously or was antagonised with neostigmine 50 μgkg⁻¹ at 10% or 25% recovery of the first twitch of the train-of-four. The median times to maximum block were 2.7, 2.2 and 1.5 min following cisatracurium 0.1 and 0.15 mgkg⁻¹ and atracurium 0.5 mgkg⁻¹, respectively. After cisatracurium 0.1 mgkg⁻¹ had been given, the median time to recovery of the train-of-four ratio to 0.8 ('adequate recovery') was 74 min during spontaneous recovery, 48 min after reversal with neostigmine when the first twitch of the train-of-four had returned to 10% of control and 50 min after reversal when the first twitch of the train-of-four had returned to 25% of control. These times for cisatracurium 0.15 mgkg⁻¹ and atracurium 0.5 mgkg⁻¹ were 90, 66 and 57 min and 75, 56 and 54 min, respectively. Administration of neostigmine significantly shortened the time to adequate recovery for both drugs but there were no significant differences in the case of either neuromuscular blocking drug between the groups of patients given neostigmine at 10 or 25% recovery of the first twitch of the train-of-four.     

不同麻醉下脊柱侧弯矫形术患者术中唤醒试验的比较

目的 比较不同麻醉下脊柱侧弯矫形术患者术中唤醒试验.方法 选择拟行脊柱侧弯矫形术患者40例,年龄13～ 18岁,性别不限,BMI＜ 30 kg/m2,ASA分级Ⅰ级.采用随机数字表法,将患者随机分为2组(n=20):异丙酚复合舒芬太尼组(P组)和靶控吸入七氟醚复合舒芬太尼组(S组).麻醉维持时S组靶控吸入七氟醚,呼气末靶浓度0.8％～1.5％;P组靶控输注异丙酚,血浆靶浓度3～5μg/rml,两组均靶控输注舒芬太尼,效应室靶浓度0.2 ～ 0.3 ng/ml.唤醒试验前停止输注顺阿曲库铵,下调舒芬太尼效应室靶浓度至0.1.ml;5 min后,S组停用七氟醚,P组停用异丙酚;5 min后开始唤醒试验.于唤醒试验前、唤醒成功时及唤醒成功后10 min(T0～2)时记录MAP和HR,记录唤醒时间、唤醒期间呛咳、躁动的发生情况,术后随访记录患者术中知晓的发生情况.结果 与P组比较,S组术中唤醒时间短(P＜0.05).两组术中唤醒期间MAP和HR均在正常范围内,两组比较差异无统计学意义(P＞0.05).所有患者术中唤醒试验均成功,术中唤醒期间无一例发生呛咳、躁动及术中知晓.结论 靶控吸入七氟醚复合舒芬太尼可安全有效地用于脊柱侧弯矫形术患者术中唤醒试验,且唤醒时间短于靶控输注异丙酚复合舒芬太尼麻醉,更适用于术中唤醒试验.