新斯的明拮抗国产阿曲库铵效果及对Q-T离散度的影响

目的研究不同剂量新斯的明拮抗国产阿曲库铵肌松恢复作用的效果及对QT离散度(QTd)的影响.方法30例ASA Ⅰ～Ⅱ级患者,随机分为三组,每组10例.分别给予新斯的明20μg/kg(N20组)、30μg/kg(N30组)和40μg/kg(N40组),观察拮抗阿曲库铵肌松作用恢复时间及对QTd的影响.结果新斯的明20μg/kg产生的肌松恢复效果弱于30μg/kg和40μg/kg,而30 μg/kg和40μg/kg所产生的效果相似.新斯的明20 μg/kg、30μ/kg对QTd的影响不明显,而40μg/kg新斯的明明显增大QTd.结论新斯的明剂量由20μg/kg增加到40 μg/kg,肌松恢复加快,但增大QTd.     

肌松拮抗用于短时腹腔镜手术的临床观察

目的:观察不同剂量新斯的明肌松拮抗用于短时腹腔镜手术的疗效与副作用。方法:选择60例择期行腹腔镜卵巢囊肿剥除术的患者,采用单次插管剂量罗库溴铵全身麻醉,手术结束时随机分为3组(n=20),N0组静脉注射生理盐水5 ml,N1组静脉注射新斯的明20μg/kg、阿托品10μg/kg,N2组静脉注射新斯的明40μg/kg、阿托品20μg/kg,根据临床征象判断拔除喉罩。检测手术结束时、拔除喉罩时及10 min后四联串刺激比率(train-of-four ratio,TOFR),记录麻醉时间(麻醉诱导至手术结束)、手术时间、拔除喉罩时间(手术结束至拔除喉罩),观察肌松拮抗用药10 min内心动过速、心动过缓及拔除喉罩10 min内低氧血症(吸入空气状态脉搏血氧饱和度<93%)发生情况。随访早期(0~6 h)及延迟(7~24 h)术后恶心呕吐(postoperative nausea and vomiting,PONV)发生情况。结果:3组患者年龄、体重、麻醉时间、手术时间、拔除喉罩时间、手术结束时TOFR及拔除喉罩后10 min内低氧血症发生率差异无统计学意义(P>0.05);拔除喉罩时TOFR N1组(0.87±0.10)、N2组(0.85±0.12)高于N0组(0.55±0.15,P<0.05);拔除喉罩10 min后TOFR N1组(0.88±0.08)、N2组(0.86±0.09)高于N0组(0.62±0.16,P<0.05);肌松拮抗用药10 min内心动过速及心动过缓发生率,N2组高于N0组、N1组(P<0.05);早期PONV发生率,N2组高于N0组(P<0.05);延迟PONV发生率,3组相比差异无统计学意义(P>0.05)。结论:对于短时腹腔镜手术,采用单次插管剂量罗库溴铵全麻后,推荐采用小剂量(20μg/kg)新斯的明进行肌松拮抗。     

围术期TOF监测与残余肌松潘库溴铵与维库溴铵的比较

目的研究潘库溴铵与维库溴铵术后残余肌松发生率,探讨围术期应用TOF监测降低术后残余肌松发生率的可行性.方法81例ASAⅠ～Ⅱ级成年择期手术病人,随机分为维库溴铵监测(V+M)组;维库溴铵未监测(V)组;潘库溴铵监测(P+M)组及潘库溴铵未监测(P)组4组.麻醉方法为静脉注射2.0～2.5mg/kg异丙酚,潘库溴铵或维库溴铵0.08～0.12mg/kg,3min后气管插管,麻醉维持应用50%N2O、异氟醚,间断给予芬太尼.使用TOF-GUARD监测仪监测肌松.P+M组和V+M组在TOF计数出现1～2个颤搐反应时给新斯的明0.04mg@kg-1、阿托品0.02mg@kg-1.拮抗;P组和V组根据临床反应判断是否给予拮抗及剂量.观察各组病人到ICU后残余肌松发生率(T4/T1＜0.70)及持续时间.结果4组病人到ICU后残余肌松发生率分别为V+M组23.80%、V组39.13%、P+M组42.11%、P组83.33%,P组残余肌松发生率显著高于V组(P＜0.01),而且监测组残余肌松发生率显著低于未监测组(P＜0.05).4组残余肌松持续时间分别为V+M组(11.11±5.48)min、V组(30.00±15.12)min、P+M组(21.15±11.62)min、P组(44.87±31.39)min,未监测组明显长于监测组(P＜0.05).未监测组潘库溴铵及维库溴铵总的用药量分别大于监测组(P＜0.05).结论1.围术期TOF监测可明显降低残余肌松发生率;2.潘库溴铵残余肌松发生率及持续时间均显著高于维库溴铵,在无神经肌肉功能监测的情况下,应用潘库溴铵应严加注意;3.应用非去极化肌松药阻滞后进行术后肌松拮抗是必要的.     

新斯的明对维库溴铵肌松恢复的影响

研究表明新斯的明副作用与剂量有关，但其拮抗肌松作用具有一定的“饱和性”。此外，新斯的明给药时机的研究结果也存在争论。本试验拟采用维库溴铵在多次追加肌松药的情况下，观察新斯的明给药剂量和时间对肌松恢复的影响。     

罗库溴铵和维库溴铵在终末期肾衰竭病人临床药效的比较

目的　比较罗库溴铵和维库溴铵在终末期肾衰竭病人中的肌松效应。方法　 2 5例ASAⅢ级行肾移植术病人随机分为罗库溴铵组 (R组 ,15例 )和维库溴铵组 (V组 ,10例 )。麻醉诱导后分别给予 2×ED95剂量的罗库溴铵 (0 6mg/kg)或维库溴铵 (0 1mg/kg)。术中当T1恢复至 2 5 %时 ,追加 0 5×ED95剂量的罗库溴铵 (0 15mg/kg)或维库溴铵 (0 0 2 5mg/kg)。末次剂量后 ,使肌张力自然恢复或给予新斯的明拮抗。结果　初量罗库溴铵的起效时间为 (1 98± 0 4 7)min ,明显短于维库溴铵的 (3 2 5±0 82 )min。初量和追加量的罗库溴铵的肌松维持时间分别为 (4 6 87± 14 6 0 )min和 (34 86± 15 5 7)min,与维库溴铵相似。两组应用拮抗药后 ,恢复指数均显著缩短。结论　对于终末期肾衰竭病人 ,罗库溴铵的起效快于维库溴铵 ,肌松作用维持时间和恢复指数与维库溴铵相似。     

小剂量新斯的明拮抗罗库溴铵残余肌松的效果

术后残余肌松可引起上呼吸道阻塞、术后缺氧等严重并发症[1-3].临床常规应用40μg/kg新斯的明拮抗残余肌松,但有研究表明,40μg/kg新斯的明可能导致肌张力已恢复的病人肌力下降[4-5].     

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.     

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.     

美维库铵持续静滴与单次静注肌松效应及恢复过程的临床药效学观察

目的 :观察美维库铵持续静滴和单次静注肌松效应及术后恢复的临床药效学指标。方法 :6 0例ASA分级Ⅰ～Ⅱ级复合全麻患者随机分为四组 ,每组 15例。美维库铵 0 2 5mg/kg给药后行气管插管 ,Ⅰ、Ⅱ组以微量泵持续静滴美维库铵 ,Ⅲ、Ⅳ组单次静注美维库铵维持肌松。术后Ⅰ、Ⅲ组患者待肌松自主恢复 ,Ⅱ、Ⅳ组静注新斯的明5 0 μg/kg、阿托品 10 μg/kg拮抗。结果 :实验提示 0 2 5mg/kg的美维库铵剂量可于 2 4± 0 6分钟内产生满意的插管条件 ,优秀率 95 %以上。Ⅰ、Ⅱ、Ⅲ、Ⅳ组平均用药量分别为 4 7± 1 2、5 0± 1 9、5 2± 2 2和 4 9± 1 8μg·kg-1·min-1,持续静滴组与单次静注组用药量无显著性差异 (P >0 0 5 )。Ⅰ、Ⅲ组恢复指数分别为 8 1± 2 3分钟和 8 7± 2 2分钟 (P >0 0 5 )。Ⅱ、Ⅳ组的恢复指数亦无明显差异 ,但比自然恢复组约缩短 2分钟左右。结论 :美维库铵持续静滴与单次静注用药量无明显差异 ,持续静滴可获得较好的肌松效果。术后使用新斯的明拮抗虽可加快肌缩力的恢复 ,但因其短效作用 ,故术后无需常规拮抗。     

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%。     

Sugammadex比新斯的明更快逆转维库溴铵所致神经肌肉阻滞的多中心随机对照研究

背景 Sugammadex是一种具有特异结构的γ-环糊精,能选择性地与肌松药结合快速逆转罗库溴铵所致的神经肌肉阻滞,并较小程度地逆转维库溴铵所致的神经肌肉阻滞.该研究中,我们对比了行择期手术的患者中sugammadex和新斯的明对逆转维库溴铵所致神经肌肉阻滞的作用.方法 年龄≥18岁,ASA分级Ⅰ～Ⅲ级拟行择期手术的患...     

Early and late reversal of rocuronium and vecuronium with neostigmine in adults and children.

We investigated the influence of the timing of neostigmine administration on recovery from rocuronium or vecuronium neuromuscular blockade. Eighty adults and 80 children were randomized to receive 0.45 mg/kg rocuronium or 0.075 mg/kg vecuronium during propofol/fentanyl/N2O anesthesia. Neuromuscular blockade was monitored by train-of-four (TOF) stimulation and adductor pollicis electromyography. Further randomization was made to control (no neostigmine) or reversal with 0.07 mg/kg neostigmine/0.01 mg/kg glycopyrrolate given 5 min after relaxant, or first twitch (T1) recovery of 1%, 10%, or 25%. Another eight adults and eight children received 1.5 mg/kg succinylcholine. At each age, spontaneous recovery of T1 and TOF was similar after rocuronium and vecuronium administration but was more rapid in children (P < 0.05). Spontaneous recovery to TOF0.7 after rocuronium and vecuronium administration in adults was 45.7 +/- 11.5 min and 52.5 +/- 15.6 min; in children, it was 28.8 +/- 7.8 min and 34.6 +/- 9.0 min. Neostigmine accelerated recovery in all reversal groups (P < 0.05) by approximately 40%, but the times from relaxant administration to TOF0.7 were similar and independent of the timing of neostigmine administration. Recovery to T1 90% after succinylcholine was similar in adults (9.4 +/- 5.0 min) and children (8.4 +/- 1.1 min) and was shorter than recovery to TOF0.7 in any reversal group after rocuronium or vecuronium administration. Recovery from rocuronium and vecuronium blockade after neostigmine administration was more rapid in children than in adults. Return of neuromuscular function after reversal was not influenced by the timing of neostigmine administration. These results suggest that reversal of intense rocuronium or vecuronium neuromuscular blockade need not be delayed until return of appreciable neuromuscular function has been demonstrated. Implications: These results suggest that reversal of intense rocuronium or vecuronium neuromuscular blockade need not be delayed until return of appreciable neuromuscular function has been demonstrated. Although spontaneous and neostigmine-assisted recovery is more rapid in children than in adults, in neither is return of function as rapid as after succinylcholine administration.     

Recovery from vecuronium neuromuscular blockade following neostigmine administration in infants, children, and adults during halothane anesthesia

To determine whether neostigmine had different effects in pediatric patients during vecuronium neuromuscular blockade, the rate of recovery following neostigmine administration was compared in infants (n = 8), children (n = 10), and adults (n = 10) during nitrous oxide-halothane anesthesia. After induction of anesthesia, patients received 100 micrograms/kg of vecuronium. The EMG response of the adductor pollicis was monitored after train-of-four (TOF) stimulation of the ulnar nerve every 20 s. When the first twitch of TOF spontaneously recovered to 10% of control value, neostigmine was injected (40 micrograms/kg in adults, 30 micrograms/kg in infants and children). During the first few minutes following neostigmine administration, no differences were observed between the three groups. After the 8 min, recovery was more rapid in children than in infants and adults up to and including the 15th min. Ten minutes after neostigmine administration, the first twitch (mean +/- SD) reached 97 +/- 3%, 99 +/- 2%, and 97 +/- 5% of control value in infants, children, and adults, respectively; TOF ratio was greater in children (0.96 +/- 0.03) than in either adults (0.82 +/- 0.17) or in infants (0.83 +/- 0.14) (P less than 0.05). During the first minutes after neostigmine administration, the lack of difference in TOF recovery in the three groups suggests that neostigmine is the main factor of recovery. In contrast, the more complete recovery after the eighth minute in children could be due to the faster rate of spontaneous recovery from vecuronium induced neuromuscular blockade in children.     

Conditions to optimise the reversal action of neostigmine upon a vecuronium-induced neuromuscular block

Background: Since neostigmine was introduced for reversal of neuromuscular block, there has been controversy about the optimum dose for antagonizing neuromuscular block. The purpose of this study was to characterise recovery of neuromuscular transmission following a vecuronium-induced block 15 min after neostigmine administration using different stimulation patterns, and to determine the effects of different doses of neostigmine given at various pre-reversal twitch heights. Methods: Adductor pollicis (AP) mechanical activity in response to low (0.1 and 2 Hz) and high (50 and 100 Hz) frequency stimulation, was recorded 15 min after 20, 40 and 80 μg/kg neostigmine, given to reverse a vecuronium-induced block at 10, 25 and 50% pre-reversal twitch height (TH). Fifty four ASA class I and II anaesthetised (methohexital, fentanyl, N₂O/O₂) young adult patients were studied and randomly allocated into 9 groups of 6 patients each. Results: In contrast to twitch height (TH) and residual force after 50 Hz, 5 s tetanic stimulation (RF50_Hz), the greater sensitivity of train-of-four (TOF) ratio and residual force after 100 Hz, 5 s tetanic stimulation (RF100_Hz) points out the best reversal conditions (prereversal TH and the optimal neostigmine dose) (P<0.001, two-way analysis of variance). The highest reversal scores (about 0.9 TOF ratio and RF100_Hz) were obtained when 40 μg/ kg of neostigmine was given at 25 and 50% TH. A 0.9 TOF ratio was also observed when 40 μg/kg of neostigmine was given at 10% TH, but, under these conditions, RF100_Hz was only 0.6 (P<0.05, Duncan test). Conclusion: To optimise the reversal action of neostigmine in order to obtain the highest neuromuscular transmission recovery (0.9 TOF ratio and RF100_Hz) during a vecuronium-induced neuromuscular block, the 40 μg/kg dose has to be given at 25 to 50% recovery of TH.     

Edrophonium and Neostigmine for Reversal of the Neuromuscular Blocking Effect of Vecuronium

The effect of edrophonium for reversal of the non-depolarizing neuromuscular blockade produced by a continuous infusion of vecuronium was compared to that of neostigmine in 20 adult patients during neurolept anaesthesia. When antagonism was attempted at 10% twitch height recovery, reversal time to a train-of-four ratio of 0.7 was significantly shorter following neostigmine 0.04 mg/kg than after edrophonium 0.75 mg/kg (9.8 min and 18.7 min, respectively) but the same after edrophonium 1.5 mg/kg (10.3 min). There was no statistically significant difference in reversal time between neostigmine 0.04 mg/kg given at 10% twitch height and edrophonium 0.75 mg/kg given at 25% twitch height recovery (6.0 min). Additional doses of atropine were necessary following edrophonium 1.5 mg/kg.     

Recovery times following edrophonium and neostigmine reversal of pancuronium, atracurium, and vecuronium steady-state infusions

The ability of edrophonium and neostigmine to antagonize nondepolarizing neuromuscular blockade produced by steady-state infusions of atracurium, pancuronium, and vecuronium was studied in 71 adult patients anesthetized with nitrous oxide and halothane. Infusion rates of blocking drugs were adjusted so that single twitch depression as measured by the evoked integrated EMG of the hypothenar muscles was kept at 10% of control. Two minutes after the termination of the infusion either edrophonium (0.75 mg/kg) or neostigmine (0.05 mg/kg) was administered. Single twitch depression and train-of-four (T4/T1) fade was recorded during the recovery period. T4/T1 fade ratios observed at 20 min postreversal were 0.80 (atracurium-edrophonium); 0.76 (vecuronium-edrophonium); 0.44 (pancuronium-edrophonium); 0.95 (atracurium-neostigmine); 0.89 (vecuronium-neostigmine); and 0.68 (pancuronium-neostigmine). Under conditions of this study neostigmine produced more rapid and complete recovery than did edrophonium. Although edrophonium produced adequate antagonism of atracurium if 20-30 min were allowed to elapse, edrophonium reversal of pancuronium was rarely acceptable even at 30 min. Increasing the dose of edrophonium to 1.0 mg/kg produced single twitch values of 0.90 at 5 min postreversal but did not increase the rate of recovery of the train-of-four fade ratio. Neostigmine reversal of pancuronium, on the other hand, generally produced T4/T1 ratios of greater than 0.70 in 20-30 min. Although the pattern of recovery seen after reversal of vecuronium was in general quite similar to that seen after atracurium, two patients in the vecuronium-edrophonium group showed delayed recovery and also failed to respond significantly to subsequent doses of neostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Neuromuscular blockade using vecuronium in dermatomyositis

The significant features of neuromuscular blockade with vecuronium in a patient with dermatomyositis are described: vecuronium 0.08 mg/kg resulted in 90%, 0.12 mg/kg in 100% neuromuscular blockade. In contrast to claims made in some previous publications, dermatomyositis did not produce increased sensitivity to vecuronium. Onset time and duration of action were also within normal limits in our patient. Time of spontaneous recovery until antagonism with neostigmine was markedly prolonged, but the dermatomyositis was only one of various possible explanations. Although there are potential hazards in the use of neostigmine in patients with dermatomyositis, antagonism of the neuromuscular block with 2 mg neostigmine was without problems in our patient. Our data support recent suggestions to reconsider the implications of dermatomyositis for anesthesia.     

Neostigmine and edrophonium antagonism of varying intensity neuromuscular blockade induced by atracurium, pancuronium, or vecuronium

To compare the time course of neostigmine and edrophonium antagonism of varying intensity neuromuscular blockade induced by atracurium, pancuronium, or vecuronium, the authors studied 98 patients anesthetized with nitrous oxide (60%) and halothane or enflurane. Neuromuscular blockade, as monitored by single stimulus-induced twitch tension (TT), was antagonized at varying degrees of spontaneous recovery (2-80% of control TT). Time to antagonism (time from injection of neostigmine or edrophonium to 90% recovery of control TT) was not different between edrophonium, 0.5 mg/kg, and neostigmine, 0.04 mg/kg, when spontaneous recovery had been allowed to occur to at least 11% of control TT prior to antagonist administration (P greater than 0.05). For profound neuromuscular blockade (TT less than or equal to 10% of control) induced by pancuronium or vecuronium, time (mean +/- SD) to antagonism with neostigmine, 0.04 mg/kg, was 7.0 +/- 2.2 min and 5.6 +/- 1.7 min, respectively, while the same for edrophonium, 0.5 mg/kg, was 20.0 +/- 8.0 min and 15.0 +/- 12.5 min, respectively (P less than 0.05). Time to antagonism of profound atracurium-induced neuromuscular blockade was 8.5 +/- 3.3 min for neostigmine, 0.04 mg/kg, and 9.8 +/- 7.0 min for edrophonium, 0.5 mg/kg, (P less than 0.05). For profound vecuronium-and pancuronium-induced neuromuscular blockade, time to antagonism by edrophonium, 1.0 mg/kg, was 4.6 +/- 3.0 min and 3.9 +/- 1.6 min respectively. The authors conclude that neostigmine, 0.04 mg/kg, antagonizes neuromuscular blockade within 12 min when TT is greater than 2% of control at time of reversal. When TT is greater than 10% of control, edrophonium, 0.5 mg/kg, produces similar time to antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dose-response relationships for edrophonium and neostigmine as antagonists of atracurium and vecuronium neuromuscular blockade

To determine the potencies of edrophonium and neostigmine as antagonists of nondepolarizing neuromuscular blockade produced by atracurium and vecuronium, dose-response curves were constructed for both antagonists when given at 10% spontaneous recovery of first twitch height. Ninety ASA physical status 1 and 2 adults were given either 0.4 mg/kg atracurium or 0.08 mg/kg vecuronium during thiopental-nitrous oxide-enflurane anesthesia. Train-of-four stimulation was applied to the ulnar nerve every 12 s, and the force of contraction of the adductor pollicis muscle was recorded. When spontaneous recovery of first twitch height reached 10% of its initial control value, edrophonium (0.1, 0.2, 0.4, or 1 mg/kg) or neostigmine (0.005, 0.01, 0.02, or 0.05 mg/kg) was administered by random allocation. Neuromuscular function in another ten subjects was allowed to recover spontaneously. Assisted recovery was defined as actual recovery minus mean spontaneous recovery observed in patients who were not given antagonists. First twitch recovery was initially more rapid when vecuronium was antagonized compared with atracurium, but no difference was detected after 10 min. At 10 min the neostigmine ED80 was 0.022 +/- 0.003 (SEM) mg/kg after atracurium and 0.024 +/- 0.003 mg/kg after vecuronium. The edrophonium ED80 was 0.44 +/- 0.11 mg/kg with atracurium and 0.46 +/- 0.12 mg/kg with vecuronium, giving a neostigmine:edrophonium potency ratio of 20. Atracurium train-of-four fade could be antagonized more easily with edrophonium, whereas that of vecuronium was more easily antagonized by neostigmine. It is concluded that edrophonium and neostigmine are not equally effective against atracurium and vecuronium.