异氟醚吸入麻醉与异丙酚静脉麻醉下长时间持续输注罗库溴铵的肌松作用

目的比较异氟醚吸入麻醉与异丙酚静脉麻醉下长时间持续输注罗库溴铵的肌松作用。方法拟在全麻下行口腔-颌面肿瘤择期手术(手术时间达5 h左右)病人30例,ASAⅠ或Ⅱ级,年龄18～65岁,随机分为2组(n=15):异丙酚组(Ⅰ组)异氟醚组(Ⅱ组)。用TOF-Watch SX肌松监测仪进行拇内收肌肌松监测。静脉注射罗库溴铵初始剂量0．6 mg·kg-1后气管插管,持续输注罗库溴铵。调整罗库溴铵的输注速率,T1稳定在基础值的10％时(初始状态),Ⅰ组靶控输注异丙酚维持麻醉,Ⅱ组吸入1 MAC异氟醚维持麻醉,持续5 h,术中维持T1在基础值的10％。记录罗库溴铵输注速率、恢复指数(T1恢复25％至75％的时间,T25-75)以及罗库溴铵停止输注到TOFR为0．9的时间。结果与初始状态比较,Ⅰ、Ⅱ组持续给药30 min-5 h时罗库溴铵输注速率下降(P<0．05);Ⅱ组持续给药1～5 h时罗库溴铵输注速率低于Ⅰ组(P<0．05)。两组间恢复指数和罗库溴铵停止输注到TOFR为0．9的时间差异无统计学意义(P>0．05)。结论罗库溴铵可用于长时间持续输注以维持稳定的肌松。维持T1在基础值的10％的情况下,持续输注罗库溴铵5 h时异氟醚麻醉比异丙酚为主的全凭静脉麻醉罗库溴铵输注速率减少30％,但其恢复指数无差异。     

丙泊酚靶控输注或异氟醚吸入对罗库溴铵药效学的影响

目的　探讨丙泊酚靶控输注和异氟醚吸入对罗库溴铵药效学的影响。方法　选择无神经肌肉疾患 ,在全麻下择期手术的病人 4 8例 ,随机分成丙泊酚靶控输注组 (B组 )和异氟醚吸入组(Y组 )维持麻醉。采用TOF刺激方式监测拇内收肌的收缩反应。当T1恢复至对照值的 2 0 %时追加罗库溴铵 0 15mg/kg。记录每次追加罗库溴铵的间隔时间以及肌松恢复情况。 结果　两组肌松维持时间无明显差异 (P >0 0 5 ) ,而B组罗库溴铵总用药量明显高于Y组 (P <0 0 5 )。B组各次追加罗库溴铵间隔时间平均为 (2 6 1± 9 3)s,Y组平均间隔时间为 (36 2± 13 2 )s,明显比B组长 (P<0 0 5 )。Y组第 1、2次给药后的间隔时间相似 (P >0 0 5 ) ,第 3、4、5次给药后间隔时间也相似 (P <0 0 5 ) ,但是比第 1、2次延长 (P <0 0 5 )。Y组T1恢复到对照值的 2 5 %、5 0 %和 75 %的时间及拔管时间比B组长 (P <0 0 5 ) ,但两组的恢复指数相似 (P >0 0 5 )。结论　丙泊酚靶控输注对罗库溴铵的药效学没有影响。而异氟醚对罗库溴铵则起增效作用 ,异氟醚维持麻醉时应酌情减少罗库溴铵的用量。     

地氟醚、异氟醚对罗库溴铵强化作用的时间依赖性研究

目的：观察IMAC地氟醚或异氟醚对罗库溴铵强化作用的时间依赖性。方法：24例择期腹部手术病人在咪唑安定－芬太尼－异丙酚麻醉期间持续输注罗库溴铵，维持95％的肌松，达到稳态后，病人随机吸入呼气末浓度为1MAC的地氟醚或异氟醚，调整罗库溴铵的注入速率，维持95％的肌松，观察吸入地氟醚或异氟醚后罗库溴铵的注入速率随时间变化的趋势。结果：地氟醚，异氟醚都显著降低了罗库溴铵的注入速率，此效应随吸入地氟醚或异氟醚时间的延长逐渐加，吸入地氟醚或异氟醚90min后达最大效应即罗库溴铵的注入速率下降到最大值。最大下降率：地氟醚组为42．7％，异氟醚组为37．6％，结论：地氟醚，异氟醚明显增强罗库溴铵的肌松作用，其程度相近，且这种强化作用有显著的时间依赖性。     

丙泊酚靶控输注和异氟醚麻醉对罗库溴铵药效学的影响

目的比较丙泊酚靶控输注（TCI）复合雷米芬太尼全凭静脉麻醉和异氟醚复合雷米芬太尼麻醉对单次插管剂量罗库溴铵肌松效应的影响。方法ASAⅠ或Ⅱ级的择期全麻患者48例,随机均分为丙泊酚（P）组和异氟醚（I）组。麻醉诱导后予0.6mg／kg的罗库溴铵插管;P组和I组麻醉维持分别采用丙泊酚TCI-泵注雷米芬太尼和吸入1 MAC异氟醚-泵注雷米芬太尼。监测脑电双频指数（BIS）,使用加速度肌松监测仪观察拇内收肌的收缩反应,记录罗库溴铵的起效时间、无反应时间、肌松维持时间及恢复指数等指标。结果两组之间肌松起效时间、无反应时间及T1 25％时间差异无统计学意义,I组25％四个成串刺激比（TOFr）及恢复指数都比P组明显延长（P〈0．05）。结论单次插管剂量的罗库溴铵在丙泊酚TCI-泵注雷米芬太尼麻醉下肌松维持及恢复无明显变化,而在吸入1 MAC异氟醚-泵注雷米芬太尼麻醉下恢复时间明显延长。     

不同浓度异氟醚对罗库溴铵肌松作用的影响

目的 观察不同浓度异氟醚对罗库溴铵肌松作用的影响。方法 60例ASA Ⅰ-Ⅱ择期手术患者,随机分为3组,每组20例。组Ⅰ静脉注射罗库溴铵0.6 mg·kg-1;组Ⅱ吸入0.6％异氟醚后静脉注入罗库溴铵0.6mg·kg-1;组Ⅲ吸入1.2％异氟醚后从静脉注入罗库溴铵0.6mg·kg-1。分别记录各组注药后肌松作用的起效时间、作用时间及T1恢复时间。结果 与组Ⅰ相比,组Ⅱ、Ⅲ起效时间明显缩短(P<0.05),TOF无反应期明显延长(P<0.01),T1恢复25％、50％、90％时间明显延长(P<0.01),且组Ⅲ较组Ⅱ延长(P<0.05),恢复指数明显延长,且组Ⅲ较组Ⅱ延长(P<0.05)。结论 吸人异氟醚能明显缩短罗库溴铵起效时间,延长罗库溴铵作用时间,临床合并使用时应注意减少用量。     

054滴注罗库溴铵对氟烷、异氟醚或七氟醚麻醉下儿童的影响

罗库溴铵是蓄积作用不明显的中效非去极化肌松药,可以持续滴注。氟烷、异氟醚、七氟醚以及地氟醚都能增强罗库溴铵的肌松效果。作者为了研究儿童在芬太尼-氧化亚氮、氟烷、异氟醚或七氟醚麻醉时,连续滴注罗库溴铵的用量问题,特选择40例体质良好的3～11岁儿童(ASA Ⅰ～Ⅱ级)随机分成4组,术前均口服咪达唑伦0.3 mg·kg-1。①FN组(芬     

罗库溴铵的自动化反馈控制给药

目的：本实验设计了一种比例－积分（ＰＩ）控制器，自动化反馈控制罗库溴铵的持续静脉输注，并研究了吸入麻醉药七氟醚对罗库溴铵的肌松作用的影响。方法：选择１４例ＡＳＡ分级Ⅰ～Ⅱ级的手术病人，随机分成七氟醚麻醉组（７例）和芬太尼复合麻醉组（７例）两组。０．６ｍｇ／ｋｇ（２×ＥＤ９５）罗库溴铵静注气管插管后，ＰＩ控制器开始控制罗库溴铵的持续静脉输注，将肌松维持在设定点ＴＨ＝５％的水平。结果：维持９５％的神经肌肉阻滞，芬太尼复合麻醉组罗库溴铵的持续输注速率为８．６±１．１μｇ·ｋｇ－１·ｍｉｎ－１；七氟醚组为４．７±１．２μｇ·ｋｇ－１·ｍｉｎ－１。七氟醚显著地降低了罗库溴铵的输注需要量（Ｐ＜０．０１）。控制器性能指标平均超调七氟醚组为０．６０％±０．４６％，复合麻醉组为０．４２％±０．６７％；平均标准差分别为１．８０％±０．６８％和２．１６％±０．７５％。结论：控制器能够将肌松控制在稳态水平，且能满足手术所要求的较高肌松水平。七氟醚显著地强化了罗库溴铵的肌松作用。     

琥珀胆碱对罗库溴铵肌松作用的影响

目的：本试验应用ＰＩ控制器自动化反馈控制罗库溴铵的输注,将肌松维持在恒定水平,通过确定罗库溴铵的稳态输注速率,来研究琥珀胆碱对罗库溴铵肌松作用的影响。方法：选择１４例ＡＳＡ分级Ⅰ～Ⅱ级的手术病人,随机分成对照组（７例）和试验组（７例）。对照组在麻醉诱导后,静注０．６ｍｇ／ｋｇ罗库溴铵进行气管插管;试验组则静注１．５ｍｇ／ｋｇ琥珀胆碱后气管插管,待肌松作用完全恢复后,再静注０．６ｍｇ／ｋｇ罗库溴铵,     

性别因素对七氟醚增强顺阿曲库铵或罗库溴铵肌松效应的影响

目的 探讨性别因素对七氟醚增强顺阿曲库铵或罗库溴铵肌松效应的影响.方法 择期全麻手术患者240例,年龄20～60岁,ASA分级Ⅰ或Ⅱ级,BMI 20～30 kg/m2,随机分为2组(n=120):顺阿曲库铵组和罗库溴铵组,各组按性别和麻醉药再分4个亚组(n=30):女性异丙酚组、男性异丙酚组、女性七氟醚组和男性七氟醚组.各异丙酚组靶控输注异丙酚,血浆靶浓度2～6 μg/ml,各七氟醚组吸入七氟醚,于靶控输注或待呼气末七氟醚浓度稳定于1.71%5 min后,静脉注射顺阿曲库铵0.15 mg/kg或罗库溴铵0.6 mg/kg.记录肌松起效时间、肌松作用峰值时间、T1 25%恢复时间和TOFR25%恢复时间.结果 与异丙酚麻醉比较,女性患者七氟醚麻醉时,罗库溴铵TOFR 25%恢复时间延长,顺阿曲库铵肌松作用峰值时间、T1 25%恢复时间和TOFR 25%恢复时间延长,男性患者七氟醚麻醉时,罗库溴铵起效时间缩短,肌松作用峰值时间、T1 25%恢复时间和TOFR 25%恢复时间延长,顺阿曲库铵肌松作用峰值时间、T1 25%恢复时间和TOFR 25%恢复时间延长(P＜0.05或0.01);七氟醚麻醉时与男性患者比较,女性患者罗库溴铵T1 25%恢复时间和TOFR 25%恢复时间缩短,顺阿曲库铵起效时间缩短(P＜0.05或0.01).结论 七氟醚对罗库溴铵肌松的增强作用存在性别差异,男性强于女性;对顺阿曲库铵肌松的增强作用无明显性别差异.     

不同液相浓度七氟醚和异氟醚对罗库溴铵结合骨骼肌成人型乙酰胆碱受体的影响

目的探讨不同液相浓度的挥发性麻醉药七氟醚、异氟醚对非去极化肌松药罗库溴铵抑制骨骼肌成人型乙酰胆碱受体(ε-nAChR)内向电流的影响。方法通过脂质体转染建立表达ε-nAChR的HEK293细胞,用全细胞膜片钳检测乙酰胆碱(Ach)激动受体峰电流。计算七氟醚、异氟醚、罗库溴铵抑制受体的半数有效抑制浓度(IC50)。分别用浓度为IC5、0.5IC50、IC50的液相七氟醚、异氟醚预处理ε-nAChR,记录0.5IC50浓度的罗库溴铵对受体内向电流的抑制率。各组以单独使用相应浓度罗库溴铵作为对照。结果七氟醚、异氟醚、罗库溴铵的IC50值分别为:(824.27±14.73)μmol/L;(1031.53±62.91)μmol/L、(150.45±12.5)μmol/L。三种浓度七氟醚、异氟醚增强罗库溴铵抑制Ach诱发电流的幅度不同,呈浓度依赖性(P<0.05);两种吸入麻醉药增强0.5IC50浓度罗库溴铵拮抗受体的作用相似。结论七氟醚、异氟醚增强罗库溴铵对ε-nAChR的阻滞作用呈浓度依赖性,且作用相似。     

A comparison of antagonism of rocuronium-induced neuromuscular blockade during sevoflurane and isoflurane anaesthesia

Volatile anaesthetic agents potentiate neuromuscular blocking agents and retard their rate of reversal. We hypothesised that there was a difference in the rate of reversal of rocuronium-induced neuromuscular blockade based on the selection of inhalation agent. Thirty-eight patients undergoing elective surgical procedures received either sevoflurane or isoflurane, by random allocation. Neuromuscular blockade was induced using rocuronium 0.6 mg.kg-1 followed by continuous intravenous infusion to maintain 90% suppression of the single twitch response. Upon completion of surgery, the rocuronium infusion was discontinued, neostigmine 50 microg.kg-1 and glycopyrrolate 10 microg.kg-1 were administered. Times from reversal to T1 = 25, 50 and 60% and train-of-four ratio = 0.6 were recorded. The mean (SD) times to train-of-four ratio = 0.6 in the isoflurane and sevoflurane groups were 327 (132) and 351 (127) s, respectively. The mean (SD) times to single twitch response T1 = 25, 50 and 60% in the isoflurane group were 81 (33), 161 (59) and 245 (84) s, respectively, and in the sevoflurane group were 95 (35), 203 (88) and 252 (127) s, respectively. It is concluded that reversal of rocuronium-induced neuromuscular blockade is similar during isoflurane and sevoflurane anaesthesia.     

七氟烷对罗库溴铵、维库溴铵及阿曲库铵临床药效的影响

目的 以丙泊酚为对照,观察1.3 MAC的七氟烷对罗库溴铵、维库溴铵及阿曲库铵临床药效的影响.方法 选择60例择期腹部手术的病人随机分为6组,每组10人.七氟烷罗库溴铵组(sR组)、七氟烷维库溴铵组(SV组)及七氟烷阿曲库铵组(SA组)分别吸入1.3 MAC的七氟烷及静注芬太尼维持麻醉,丙泊酚罗库溴铵组(CR组)、丙泊酚维库溴铵组(CV组)及丙泊酚阿曲库铵组(CA组)以丙泊酚6 mg·kg-1·h-1～8 mg·kg～·h-1及芬太尼维持麻醉.监测起效时间、最大抑制程度、作用时间、维持速率、恢复时间、恢复指数.结果 七氟烷组与相应的对照组在最大抑制程度、恢复指数方面的无统计学差异,起效时间、作用时间、维持速率、恢复时间有统计学差异.结论 七氟烷能明显延长罗库溴铵、维库溴铵以及阿曲库铵的作用时间和恢复时间并减少其起效时间、维持剂量,但对最大抑制程度和恢复指数则无明显影响.     

Reversal of rocuronium-induced (1.2 mg/kg) profound neuromuscular block by sugammadex: a multicenter, dose-finding and safety study

BACKGROUND: Reversal of rocuronium-induced neuromuscular blockade can be accomplished by chemical encapsulation of rocuronium by sugammadex, a modified gamma-cyclodextrin derivative. This study investigated the efficacy and safety of sugammadex in reversing rocuronium-induced profound neuromuscular blockade at 5 min in American Society of Anesthesiologists physical status I and II patients. METHODS: Forty-five American Society of Anesthesiologists physical status I and II patients (aged 18-64 yr) scheduled to undergo surgical procedures (anticipated anesthesia duration >/= 90 min) were randomly assigned to a phase II, multicenter, assessor-blinded, placebo-controlled, parallel, dose-finding study. Anesthesia was induced and maintained with propofol and an opioid. Profound neuromuscular blockade was induced with 1.2 mg/kg rocuronium bromide. Sugammadex (2.0, 4.0, 8.0, 12.0, or 16.0 mg/kg) or placebo (0.9% saline) was then administered 5 min after the administration of rocuronium. Neuromuscular function was monitored by acceleromyography, using train-of-four nerve stimulation. Recovery time was the time from the start of administration of sugammadex or placebo, to recovery of the train-of-four ratio to 0.9. Safety assessments were performed on the day of the operation and during the postoperative and follow-up period. RESULTS: A total of 43 patients received either sugammadex or placebo. Increasing doses of sugammadex reduced the mean recovery time from 122 min (spontaneous recovery) to less than 2 min in a dose-dependent manner. Signs of recurrence of blockade were not observed. No serious adverse events related to sugammadex were reported. Two adverse events possibly related to sugammadex were reported in two patients (diarrhea and light anesthesia); however, both patients recovered without sequelae. CONCLUSIONS: Sugammadex rapidly and effectively reversed profound rocuronium-induced neuromuscular blockade in humans and was well tolerated.     

肝移植术患者罗库溴铵不同给药方式肌松效果的比较

目的 比较肝移植术患者间断静脉注射(Ⅳ)、静脉输注(CI)和靶控输注(TCI)罗库溴铵的肌松效果.方法 拟行肝移植术的患者36例,性别不限,年龄21～63岁,体重48～80 kg,Child-Pugh评分7～9分,肝功能Child分级B或C级,随机分为3组(n=12):Ⅳ组、CI组和TCI组.采用TOF模式进行肌松监测,Ⅳ组:麻醉诱导时静脉注射罗库溴铵0.6 mg/kg,无肝前期T1恢复至25%时、无肝期和新肝期T4/T1(TOFR)恢复至25%时追加0.15 mg/kg.TCI组:麻醉诱导时靶控输注罗库溴铵,初始效应室靶浓度3μg/ml,调整靶浓度,维持T1 5%～10%;无肝期和新肝期开始时暂停TCI,随后以效应室靶浓度0.1μg/ml再次输注,调整靶浓度,维持T15%～10%.CI组:麻醉诱导时静脉注射罗库溴铵0.6 mg/kg,无肝前期以30μg·kg-1·min-1的速率开始静脉输注,调节输注速率,维持T1 5%～10%,无肝期和新肝期开始时暂停CI,随后以1μg·kg-1·min-1的速率静脉再次输注,调整输注速率,维持T15%～10%.各组于肌松达最大效应时行气管插管,于缝合腹膜后停止给药.记录麻醉诱导时罗库溴铵肌松起效时间、T1最大抑制程度和气管插管条件满意情况;记录各组无肝期T1 25%恢复时间及TOFR 25%恢复时间,新肝期停药后T125%恢复时间、TOFR 25%恢复时间、TOFR 75%恢复时间、TOFR90%恢复时间及恢复指数;记录罗库溴铵总用量.结果 与Ⅳ组比较,TCI组和CI组气管插管条件满意率、罗库溴铵总用量、麻醉诱导时罗库溴铵起效时间、T1最大抑制程度和各期肌松恢复情况差异均无统计学意义(P＞0.05).肌松效应监测图显示Ⅳ组各期罗库溴铵肌松效应波动较大,TCI组和CI组各期肌松效应较为平稳.结论 采用Ⅳ、CI和TCI给药时,肝移植术患者罗库溴铵肌松起效和恢复情况无差异,而采用TCI或CI给药时,肌松效应较Ⅳ更加平稳.     

Sevoflurane increases fade of neuromuscular response to TOF stimulation following rocuronium administration in children. A PK/PD analysis

BACKGROUND: Sevoflurane enhances neuromuscular block produced by rocuronium, affecting not only single twitch response but also the response to high-frequency stimulation, increasing tetanic [or train-of-four (TOF)] fade. METHODS: We compared the degree of fade during spontaneous recovery from rocuronium-induced neuromuscular block in 24 children (3-11 years old, ASA groups I and II), anesthetized with nitrous oxide-sevoflurane (one MAC, endtidal concentration) or nitrous oxide-fentanyl. Neuromuscular transmission was monitored electromyographically (EMG), stimulating the ulnar nerve at the wrist with TOF, 2 Hz for 2 s, repeated at 20-s intervals and recording EMG potential from adductor pollicis brevis. Depression of the fourth twitch, T4, was used as a measure of fade. Following an intubating dose of rocuronium, 0.6 mgxkg(-1), continuous infusion of rocuronium was given to maintain stable 90-99% T1 depression. Plasma concentration of rocuronium was determined with high performance liquid chromatography with electrochemical detection (HPLC-EC) method at the moment of discontinuation of rocuronium infusion and 10, 20, 30, 40, 50, 60, and 75 min afterwards. A two compartment model was used for pharmacokinetic (PK) calculations. PK parameters were fixed and pharmacodynamic data were fitted to effect compartment model proposed by Sheiner. RESULTS: Sevoflurane reduced rocuronium concentration in effect compartment producing 50% inhibition of both T1 and T4 response and significantly delayed not only T1, but also T4 recovery. CONCLUSIONS: Potentiating effect of sevoflurane on rocuronium-induced neuromuscular block influences not only postsynaptic, but also the presynaptic part of the neuromuscular junction, enhancing fade of neuromuscular response to high-frequency stimulation. The intensity of this latter effect is clinically relevant.     

Rocuronium pharmacokinetic-pharmacodynamic relationship under stable propofol or isoflurane anesthesia

PURPOSE: To compare the pharmacokinetics, pharmacodynamics and the concentration-effect relationship of rocuronium in patients under stable propofol or isoflurane anesthesia. METHODS: Ten patients were randomized to receive fentanyl, propofol and nitrous oxide (60%) or fentanyl, thiopental, isoflurane (1.2% end-tidal concentration) and nitrous oxide (60%). To obtain good intubation conditions and maintain adequate muscle relaxation during surgery, patients received two bolus doses of rocuronium: 0.5 mg x kg(-1) (1.7 x ED95) at induction followed one hour later by 0.3 mg x kg(-1) (1 x ED95). Arterial blood samples were obtained over six hours after the second bolus dose. Plasma concentrations of rocuronium were measured using high pressure liquid chromatography. Muscle twitch tension was monitored by mechanomyography for the two doses. Pharmacokinetic and pharmacodynamic parameters were determined. RESULTS: No differences in rocuronium pharmacokinetic parameters were observed between both groups. After the second bolus, clinical duration was 20 +/- 6 min in the propofol group vs 39 +/- 8 min in the isoflurane group (P <0.05). The effect compartment concentration corresponding to 50% block, EC50, was higher under propofol anesthesia: 1008 vs 592 microg x L(-1) (P <0.05). CONCLUSION: Rocuronium body disposition is similar under stable propofol or isoflurane anesthesia. In contrast to isoflurane, propofol does not prolong the neuromuscular block. Therefore, the potentiating effect of isoflurane is of pharmacodynamic origin only, as explained by an increased sensitivity at the neuromuscular junction. In contrast with isoflurane anesthesia where the dose of rocuronium has to be decreased under stable conditions, no dose adjustment is required under propofol anesthesia.     

An overview of the pharmacokinetics and pharmacodynamics of rocuronium bromide

For many years, much effort has been done to develop non-depolarizing neuromuscular blocking agents of rapid onset and short duration. It has been shown that rocuronium bromide is a nondepolarizing, steroidal muscle relaxant with fast onset and short-to-intermediate duration of action. In addition, rocuronium-induced neuromuscular blockade can be readily and consistently reversed following the administration of reversal agents. The pharmacology and pharmacodynamics of rocuronium bromide are summarized in this review.     

Recovery from neuromuscular blockade after either bolus and prolonged infusions of cisatracurium or rocuronium using either isoflurane or propofol-based anesthetics

We examined the recovery characteristics of cisatracurium or rocuronium after bolus or prolonged infusion under either isoflurane or propofol anesthesia. Sixty patients undergoing neurosurgical procedures of at least 5 h were randomized to receive either isoflurane with fentanyl (Groups 1 and 2) or propofol and fentanyl (Groups 3 and 4) as their anesthetic. Groups 1 and 3 received cisatracurium 0.2 mg/kg IV bolus, spontaneously recovered, after which time an infusion was begun. Groups 2 and 4 received rocuronium 0.6 mg/kg IV, spontaneously recovered, and an infusion was begun. Before the end of surgery, the infusion was stopped and recovery of first twitch (T(1)), recovery index, clinical duration, and train-of-four (TOF) recovery was recorded and compared among groups by using appropriate statistical methods. Clinical duration was shorter for rocuronium compared with cisatracurium using either anesthetic. Cisatracurium T(1) 75% recovery after the infusion was shorter with propofol compared with isoflurane. Cisatracurium TOF 75% recovery was similar after either bolus or infusion, but rocuronium TOF 75% recovery after the infusion was delayed. Infusion rates decreased for cisatracurium but remained relatively constant for rocuronium regardless of the anesthetic used. Isoflurane enhances the effect of both muscle relaxants but prolonged cisatracurium recovery more than rocuronium. Of the two muscle relaxants studied, rocuronium's recovery was most affected by length of the infusion. Cisatracurium may be a more desired muscle relaxant for prolonged procedures because recovery was least affected by prolonged infusion. Implications: This study describes the effect of different anesthetic techniques on the recovery of two different muscle relaxants, cisatracurium and rocuronium, when administered as either a single bolus or prolonged infusion during neurosurgery. This study demonstrates the feasibility of using these relaxants for these prolonged procedures.     

The influence of halothane, isoflurane and sevoflurane on rocuronium infusion in children

BACKGROUND: Rocuronium is a non-depolarizing neuromuscular blocking agent with intermediate duration of action and without significant cumulative properties, suitable for continuous infusion. This study was designed to determine the infusion requirements in children under nitrous oxide and fentanyl, halothane, isoflurane or sevoflurane anaesthesia. METHODS: Forty children, 3-11 years old, ASA physical status group I or II were studied. They were randomly allocated to receive fentanyl-nitrous oxide, 1 MAC halothane-nitrous oxide, 1 MAC isoflurane-nitrous oxide or 1 MAC sevoflurane-nitrous oxide anaesthesia. Rocuronium, 0.6 mg(-1) was used to facilitate endotracheal intubation. Electromyographic response of adductor pollicis to train-of-four (TOF) stimulation, 2 Hz for 2 s, applied to the ulnar nerve at 10-s intervals was recorded using Relaxograph (Datex, Helsinki, Finland). Once the first twitch response (T1) returned to 5%, muscle relaxation was maintained by continuous infusion of rocuronium, adjusted automatically in a closed-loop system to maintain a stable 90-99% T1 depression. The block was considered stable if it changed by no more than 2% over a 10-min observation period. RESULTS: Halothane, isoflurane and sevoflurane groups had ower infusion requirements than the fentanyl-nitrous oxide group (P<0.00075). Rocuronium requirement (mean +/- SD) at one hour from the commencement of anaesthesia was 16.7+/-2.3, 13.6+/-3.7, 13.1+/-5.1 and 8.4+/-1.6 microg x kg(-1) x min(-1) for children receiving fentanyl-nitrous oxide, halothane, isoflurane and sevoflurane anaesthesia, respectively. CONCLUSIONS: The rocuronium infusion rate required to maintain stable 90-99% T1 depression was reduced by approximately 20% with halothane and isoflurane anaesthesia, and by 50% with evoflurane anaesthesia when compared to fentanyl-nitrous oxide anaesthesia. Significant patient-to-patient variability of infusion rate makes monitoring of neuromuscular transmission necessary.     

Successful management of rocuronium-induced anaphylactic reactions with sugammadex: a case report

Sugammadex, a new reversal agent for rocuronium, encapsulates the rocuronium molecule and results in rapid reversal of rocuronium-induced neuromuscular blockade. A case in which sugammadex was used to treat an anaphylactic reaction that occurred after rocuronium is presented. The binding/encapsulation of rocuronium by sugammadex may selectively eliminate the antigenic quaternary ammonium activity of circulating rocuronium, and prevent the propagation of rocuronium-induced anaphylaxis.