ORM1 A113G基因多态性对女性患者维库溴铵肌松效应的影响

目的探讨ORM1 A113G基因多态性对女性患者维库溴铵肌松效应的影响。方法选择择期全麻下乳腺包块切除术贵州汉族女性患者107例,年龄18~65岁。术前采集外周静脉血5ml,使用天根血液基因组DNA提取试剂盒抽取DNA。采用3730XL DNA测序仪直接测序对ORM1A113G进行基因分型。麻醉诱导期间给予维库溴铵0.1mg/kg,用TOF-Watch加速度仪进行肌松监测。观察起效时间、时效、体内作用时间、恢复指数、TOF恢复到25%的时间。结果根据基因型将患者分为野生型纯合子组(AA组,n=71)、突变型杂合子组(AG组,n=35)和突变型纯合子组(GG组,n=1)。将AG组和GG组两种基因型合并为变异组。与AA组比较,变异组的时效和TOF恢复到25%时间均明显延长(P0.05);起效时间、恢复指数和体内作用时间差异无统计学意义。结论ORM1 A113G基因多态性可在一定程度上影响贵州汉族女性患者维库溴铵的肌松效应。     

高血压患者长期口服二氢吡啶类药物对维库溴铵肌松效应的影响

目的 观察高血压患者长期口服二氢吡啶类药物对维库溴铵的肌松效应的影响.方法 选择长期口服（超过3个月）珍菊降压片或二氢吡啶类药的高血压患者行中下腹部手术各30例,ASA Ⅰ或Ⅱ级,分为两组：长期口服二氢吡啶类药组（观察组）和长期口服珍菊降压片组（对照组）.用肌松监测仪观察并记录两组患者术中维库溴铵的起效时间（T1消失）、T1出现时间、TOF出现时间、T1恢复至25%的时间及恢复指数.结果 两组患者术中维库溴铵的起效时间、作用持续时间和恢复指数差异均无统计学意义.结论 高血压患者长期使用二氢吡啶类药物对维库溴铵肌松效应无显著影响.     

硫酸镁对顺阿曲库铵肌松效应时效关系的影响

顺式阿曲库铵是阿曲库铵的同分异构体,其肌松效应约为阿曲库铵的3倍.因其起效时间较长,快速诱导气管插管时常采用增大用药剂量的方法缩短其起效时间,但易导致肌松维持和恢复时间延长.研究表明,镁离子可有效缩短维库溴铵、泮库溴铵及阿曲库铵的起效时间[1-3],而其对顺阿曲库铵的起效时间的影响尚不清楚.因此本研究拟探讨硫酸镁对顺阿曲库铵肌松效应时效关系的影响.     

老年患者全麻术后罗库溴铵的残余作用

目的观察老年患者全麻术后罗库溴铵的残余效应(PORC)。方法择期全麻手术患者40例,根据年龄分为中青年组和老年组,每组20例。采用静脉复合全麻,罗库溴铵用量为0.9mg/kg。术中用四个成串刺激(TOF)监测肌松,直至拔管后TOF值(TOFr)≥90%。记录各组TOFr从0恢复到25%(临床时效)、从25%恢复到90%的时间,以及拔管时TOFr<90%(PORC)患者TOFr恢复到90%的时间。监测拔管后及TOFr达90%时的动脉血气。结果老年组罗库溴铵作用时效[(60.70±14.27)minvs.(45.51±7.80)min]及TOFr从25%恢复至90%时间[(46.50±11.56)minvs(34.50±9.56)min]均长于中青年组(P<0.05);老年组PORC发生率高于中青年组(15/20vs12/20),PORC持续时间长于中青年组[(26.00±8.43)minvs(17.20±8.00)min](P<0.05);老年组拔管后CO2蓄积例数多于中青年组(13例vs.6例)(P<0.05)。结论老年患者罗库溴铵的PORC发生率高于中青年患者,应加强围手术期肌松监测,掌握恰当的拔管时机。     

七氟醚对不同性别患者罗库溴铵肌松作用的影响

目的 比较罗库溴铵肌松效应的性别差异和七氟醚对不同性别患者罗库溴铵肌松增效作用.方法 择期手术患者120例(男:女为1:1),年龄20～60岁.ASA Ⅰ或Ⅱ级,按性别随机分为丙泊酚组和七氟醚组:女性丙泊酚组(PF组).男性丙泊酚组(PM组),女性七氟醚组(SF组),男性七氟醚组(SM组),每组30例.所有患者静脉注射咪达唑仑、芬太尼和丙泊酚行麻醉诱导,意识消失后,置入喉罩,接麻醉机辅助通气并启动肌松监测.丙泊酚组静脉输注丙泊酚维持麻醉,设定血浆靶控浓度2～6 μg/ml,输注丙泊酚5 min后静脉注射罗库溴铵0.6 mg/kg,七氟醚组在呼气末七氟醚浓度稳定于1 MAC 5 min后静脉注射罗库溴铵0.6 mg/kg.记录肌松起效时间、完全肌松时间、T1恢复到25%和TOF恢复到25%的时间.结果 PM组较PF组起效时间长,完全肌松时间、T1恢复到25%和TOF恢复到25%的时间缩短(P＜0.05).SF组TOF恢复到25%的时间较PF组延长(P＜0.05),SM组较PM组起效时间缩短,完全肌松时间、T1恢复到25%和TOF恢复到25%的时间均延长(P＜0.05).SM组T1恢复到25%和TOF恢复到z5%的时间较SF组延长(P＜0.05).结论 女性罗库溴铵起效更快,作用时间长;而七氟醚对男性罗库溴铵的增效作用优于女性.     

尼卡地平对维库溴铵和阿曲库铵肌松时效的影响

目的探讨尼卡地平对维库溴铵、阿曲库铵肌松时效的影响.方法40例ASAⅠ～Ⅱ级择期手术的全麻患者,随机分为四组,每组10例.四组病人均行健忘镇痛慢诱导气管内插管.吸入5096N2O-氧混合气,静注芬太尼、羟丁酸钠维持麻醉.Ⅰ组静注维库溴铵0.1mg@kg-1(2×ED95);Ⅲ组静注阿曲库铵0.5mg@kg-1(2×ED95);收缩压超过基础值30%时,Ⅱ组和Ⅳ组均给予尼卡地平20μg@kg-1,1min后分别静注与Ⅰ组、Ⅲ组同等剂量的维库溴铵或阿曲库铵.用Biometer加速度仪监测肌松情况.结果Ⅰ组、Ⅱ组维库溴铵起效时间分别为(2.6±0.2)min和(2.0±0.2)min,Ⅲ组、Ⅳ组阿曲库铵起效时间分别为(3.1±0.7)min和(2.3±0.5)min,Ⅱ组和Ⅳ组均明显缩短(P＜0.05);Ⅱ组临床作用时间较Ⅰ组延长(P＜0.05);Ⅳ组T190%恢复时间及恢复指数较Ⅲ组延长(P＜0.05);Ⅱ组无反应期、T150%恢复时间、9096恢复时间及恢复指数,均长于Ⅰ组;Ⅳ组无反应期、临床作用时间及T15096恢复时间均长于Ⅲ组,但无统计学意义).结论尼卡地平能缩短维库溴铵、阿曲库铵的起效时间,延长维库溴铵、阿曲库铵的临床作用和恢复时间.     

肝硬化病人乌司他丁预处理对罗库溴铵肌松作用的影响

目的观察肝硬化病人乌司他丁预处理对罗库溴铵肌松作用的影响。方法选择30例患有肝硬化的成年手术病人,随机均分为两组:乌司他丁组(Ⅰ组),静注乌司他丁5000U/kg后1min,静脉给予罗库溴铵0.6mg/kg;生理盐水组(Ⅱ组),静脉给予生理盐水0.1ml/kg后1min,静脉给予罗库溴铵0.6mg/kg。另选15例无肝脏疾患的、ASAⅠ～Ⅱ级择期成年手术病人为对照组(Ⅲ组),处理同Ⅱ组。肌松监测仪检测四个成串刺激(TOF)的变化,记录三组注药后罗库溴铵的起效时间(注药到TOFr=0)、TOF无反应时间(T1=0持续时间)、T1最大抑制程度、临床时效(TOFr恢复至25%时间)、T1恢复至75%时间、恢复指数。结果与Ⅱ、Ⅲ组比较,Ⅰ组插管剂量罗库溴铵的起效时间明显延长(P<0.05)。Ⅱ、Ⅲ组罗库溴铵肌松的起效时间相似。与Ⅱ组比较,Ⅰ、Ⅲ组T1恢复25%时间和恢复指数明显缩短(P<0.05)。Ⅰ、Ⅲ组罗库溴铵肌松的恢复时间相似。结论肝硬化病人乌司他丁预处理延长罗库溴铵的起效时间,但缩短罗库溴铵肌松作用时间。     

急性高容量血液稀释对全麻患者维库溴铵肌松起效和恢复的影响

目的 探讨急性高容量血液稀释(AHHD)对全麻患者维库溴铵肌松起效和恢复的影响.方法 择期全麻下普通外科手术患者32例,ASA Ⅰ或Ⅱ级,随机分为2组(n=16):对照组和AHHD组.AHHD组AHHD完成并稳定10min后、对照组气管插管完成后,静脉注射维库溴铵负荷剂量0.1 mg/kg.静脉输注维库溴铵维持Tl/Tc 5%～15%.于AHHD前、后各时点测定血生化指标,记录维库溴铵起效时间和恢复时间.结果 与对照组比较,AHHD组AHHD后Hct、Hb、血浆总蛋白及白蛋白浓度降低,维库溴铵起效时间和恢复时间均缩短(P＜0.05),肝、肾和凝血功能指标差异无统计学意义(P＞0.05).结论 急性高容量血液稀释可缩短全麻患者维库溴铵的肌松起效时间,加快肌松恢复.     

地氟醚七氟醚对糖尿病患者罗库溴铵肌松效应影响的比较

目的 比较地氟醚和七氟醚对糖尿病患者罗库溴铵肌松效应的影响.方法 择期2型糖尿病腹部手术患者60例,年龄45～64岁,ASA分级Ⅱ级,采用随机数字表法分为3组,每组20例:地氟醚组(DD组)、七氟醚组(SD组)和异丙酚组(PD组).静脉注射咪达唑仑、异丙酚和芬太尼行麻醉诱导后启动肌松监测,3组分别用异丙酚、地氟醚和七氟醚维持麻醉.记录肌松维持时间和恢复指数.于静脉注射罗库溴铵后10、20、30、40、50、60、70、80、90、100、110、120 min时记录T1/T0比值及T4/T1比值[四个成串刺激(train-of-four stimulation, TOF)比值].结果 DD组和SD组患者罗库溴铵的维持时间[(61±17),(60±18) min]、恢复指数[(36±12),(35±10) min]之间差异无统计学意义(P＞0.05),且均大于PD组(P＜0.05).DD组、SD组患者静脉注射罗库溴铵后60～120 min时T1/T0比值和TOF比值差异无统计学意义(P＞0.05),且均大于PD组(P＜0.05).结论 地氟醚和七氟醚对糖尿病患者罗库溴铵肌松效应的影响差异无统计学意义.     

罗库溴铵预注和麻黄碱预处理对小儿罗库溴铵肌松起效的影响

目的 观察小儿在罗库溴铵预注、麻黄碱预处理和罗库溴铵预注复合麻黄碱预处理对罗库溴铵起效时间、插管条件和肌松时效的影响.方法 选择全麻下行择期手术的患儿80例,ASA Ⅰ或Ⅱ级,随机均分为四组.在麻醉诱导前预先静注:Ⅰ组生理盐水O.5 ml,Ⅱ组罗库溴铵0.06 mg/kg,Ⅲ组麻黄碱70 μg/kg,Ⅳ组罗库溴铵0.06 mg/kg和麻黄碱70 μg/kg.预注和预处理4min后,Ⅰ、Ⅲ组静注罗库溴铵0.6 mg/kg,Ⅱ、Ⅳ组静注罗库溴铵0.54 mg/kg.待四个成串刺激(TOF)第1个颤搐反应高度(Th)达最大阻滞程度后行气管插管.记录肌颤搐抑制75%、90%和达最大阻滞程度的时间,并评估气管插管条件,同时观察HR、BP变化.结果 Ⅰ、Ⅱ、Ⅲ、Ⅳ组的最大阻滞起效时间分别为(196±43)、(140±43)、(144±35)和(100±33)s,Ⅱ、Ⅲ、Ⅳ组的起效时间明显短于Ⅰ组(P＜0.05),Ⅳ组的起效时间较Ⅱ、Ⅲ组短(P＜0.05).各组气管插管条件均达到6～9分,优良率100%.各组麻醉诱导期间均无明显的心血管不良反应.各组的临床肌松作用时间和恢复指数差异均无统计学意义.结论 罗库溴铵预注和麻黄碱预处理分别使用均能缩短小儿罗库溴铵的肌松起效时间,而两种方法复合使用可进一步加快肌松起效,但该方法对罗库溴铵的肌松时效无明显的影响.     

七氟烷对国产顺式阿曲库铵神经肌肉深度阻滞期的影响

目的观察七氟烷吸入麻醉与丙泊酚静脉麻醉两种不同麻醉维持方法下对国产顺式阿曲库铵神经肌肉深度阻滞期的影响。方法择期行全身麻醉下胆囊切除手术患者60例,ASAⅠ~Ⅱ级,麻醉诱导插管后随机分为S组(n=30)和V组(n=30),分别采用成七氟烷+瑞芬太尼和丙泊酚+瑞芬太尼维持麻醉。使用连续肌松监测仪连续测定左手拇内收肌的四个成串刺激(TOF)值,无反应期进行强直刺激后单次刺激肌颤搐计数(PTC);记录阻滞起效时间、深度阻滞维持时间、深阻滞恢复时间、25%TOF恢复时间、95%TOF恢复时间,计算出深-浅交界阻滞时间及总体内作用时间。结果两组深度阻滞期时间比较无统计学差异(P0.05),但S组深-浅交界阻滞时间及25%TOF恢复时间明显长于V组(P0.05)。结论七氟烷加强国产顺式阿曲库铵肌松时间位于PTC首次出现到TOF 25%恢复的深-浅阻滞交界时间段,部位主要在接头后膜。     

预注不同剂量米库氯铵对肌松效应的影响

目的 观察预先注射(预注)不同剂量米库氯铵对肌松效应的影响. 方法 选择全身麻醉下行择期手术的患者40例,年龄18 ～60岁,ASA分级Ⅰ、Ⅱ级,按随机数字表法分为4组(每组10例):对照组(A组)、预注20％的95％有效药物剂量(95％ effective dose,ED95)米库氯铵组(B组)、预注30％ED95米库氯铵组(C组)、预注40％ED95米库氯铵组(D组).丙泊酚联合舒芬太尼麻醉诱导后,A组预注生理盐水,B组、C组和D组分别预注米库氯铵0.014 mg/kg(20％ED95)、0.021 mg/kg(30％ED95)和0.028 mg/kg(40％ED95),预注后2 min,给予剩余插管剂量(A组0.210 mg/kg、B组0.196 mg/kg、C组0.189 mg/kg、D组0.182 mg/kg).应用四个成串刺激(train of four stimulation,TOF)-Watch加速仪进行肌松监测.观察肌松起效时间、阻滞维持时间、临床作用时间、体内作用时间和恢复指数. 结果 与A组比较,B组、C组和D组米库氯铵起效时间显著缩短[(183±48)s比(141±18)、(132±30)、(117±21) s](P＜0.05);B组、C组和D组组间比较,起效时间差异无统计学意义(P＞0.05);4组间阻滞维持时间、临床作用时间、体内作用时间和恢复指数差异无统计学意义(P＞0.05). 结论 预注可显著缩短米库氯铵的起效时间,不影响肌松维持和恢复过程,但加大预注剂量未能明显缩短起效时间.     

Neuromuscular blockade following high-dose vecuronium administration

To determine the onset time, duration of action and recovery time of high-dose vecuronium, 70 patients were assigned to receive either 100, 150, 200 or 300 micrograms.kg-1 of vecuronium for muscle relaxation during elective surgery. Neuromuscular blockade was continuously quantitated by recording the EMG response to stimulation of the ulnar nerve. The onset time from the time of vecuronium administration to maximum blockade decreased from 4.6 +/- 1.1 to 2.4 +/- 0.5 min when the vecuronium doses increased from 100 to 300 micrograms.kg-1. Significant differences were observed in the onset time between the 100 micrograms.kg-1 dose and the other dose groups. Endotracheal intubating conditions were excellent in all patients except 3 in the 100 micrograms.kg-1 dose group. The duration of action from the time of injection to 25% recovery increased from 32 +/- 9 to 138 +/- 48 min in a dose dependent manner. The duration of action after increment doses of 40 or 50 micrograms.kg-1 up to 25% recovery of T1 did not vary significantly within the same dose group. With an initial dose of 150 micrograms.kg-1 and subsequent increment doses of 50 micrograms.kg-1 or less, the duration of action remained constant. The recovery time from 25 to 75% recovery was within 11 minutes when antagonists were administered. High-dose vecuronium may, therefore, be a useful alternative to SCC, when a rapid onset is required and to pancuronium, when a rapid recovery from neuromuscular blockade is requested.     

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.     

Atracurium: neuromuscular blockade in repeated administration

The neuromuscular blocking action of repeated injections of atracurium and vecuronium was studied in 74 surgical patients during balanced anaesthesia (methohexitone or etomidate, intubation after suxamethonium, fentanyl, droperidol, N2O). The initial bolus dose (ID) of atracurium was 0.25 mg/kg and of vecuronium 0.05 mg/kg followed by repeated increments (RD) of atracurium 0.1 mg/kg and vecuronium 0.0125 mg/kg when neuromuscular function (EMG) had recovered to about 30% of pre-relaxant control. Dose-response relationships revealed atracurium to be about 1/5 as potent as vecuronium; the ED50 of atracurium was 0.13 +/- 0.03 mg/kg and of vecuronium 0.023 +/- 0.007 mg/kg. The ID of both relaxants produced a neuromuscular blockade of about 90% within 4 min. The duration from the time of injection to 30% recovery was slightly longer in atracurium 26 +/- 9 min. In all patients the RD produced within 3.5 min satisfactory muscle relaxation with a neuromuscular block of about 85%. The mean duration of atracurium (18 min) was 5-10 min longer than of vecuronium (12 min). To maintain good surgical relaxation (more than 70% blockade) atracurium 0.32 mg/kg X h and vecuronium 0.056 mg/kg X h were required. No cumulation could be measured after repeated injections. The recovery time of atracurium and vecuronium at the end of anaesthesia was 10-12 min. Neither cardiovascular side-effects nor signs of histamine release were observed after both relaxants in our particular dose range. It is concluded, that atracurium is a favourable blocker for anaesthetic practice: The time of onset is approximately the same compared with vecuronium. The duration of action, however, is slightly longer but still truly intermediate long.(ABSTRACT TRUNCATED AT 250 WORDS)     

The neuromuscular blocking effects of ORG 9426]

ORG 9426 is a new non-depolarizing steroidal muscle relaxant with a short onset time and intermediate duration of action. Its ED90 ist estimated to be between 0.25 and 0.36 mg/kg. The present study investigated the onset time, duration of action and time to spontaneous recovery after 0.3 and 0.9 mg/kg ORG 9426, respectively (i.e. about single or triple ED90). METHODS. Following the consent of the ethics committee and informed patient consent, two groups of 18 patients (ASA I or II) were formed, each scheduled for general or ORL surgery. After premedication with lormetazepam, anesthesia was induced with midazolam (0.07 mg/kg) and etomidate (0.3 mg/kg) and maintained with N2O/O2 at a 65:35 ratio, enflurane (0.8-1.5%) and supplements of fentanyl as needed. The ulnar nerve was stimulated with supramaximal 2 Hz Train-of-four (TOF) every 20 s. Neuromuscular twitch response was registered with EMG. Muscle relaxation was achieved by administration of ORG 9426 0.3 (group 1) and 0.9 mg/kg (group 2), respectively. The following parameters were measured: onset time (time interval from injection to maximal or total block), T125/75 (time for T1 to reach 25% or 75% of control), TOF70 (time for TOF ratio to reach 70% of control), heart rate and blood pressure. RESULTS. (mean +/- SD). At a dosage of 0.3 mg/kg, the onset time was 3.1 +/- 0.8 min and the maximum blockade was 87 +/- 9%. A dosage of 0.9 mg/kg led to complete paralysis (100%) in all patients within 1.2 +/- 0.3 min. The time for recovery of T1 to 25 and 75% of baseline was 18 +/- 7 and 26 +/- 8 min in group 1, in group 2 46 +/- 11 and 53 +/- 17 min, respectively. TOF70 (i.e., time to adequate spontaneous recovery of neuromuscular function) was achieved after 30 +/- 10 and 63 +/- 14 min, respectively. CONCLUSIONS. At a dosage of 0.3 mg/kg, ORG 9426 has an onset time of about 3 min and a duration of activity of nearly half an hour. Its neuromuscular effects are similar to a single ED90 dose of vecuronium. In contrast to a previous study, we observed a much shorter onset time of 70 s following the administration of 0.9 mg/kg. The clinical duration of action and spontaneous recovery of neuromuscular function, however, were significantly prolonged to more than 1 h. The hemodynamic parameters showed only slight alterations.     

维库溴铵预注复合麻黄素预处理对麻醉诱导时维库溴铵的起效时间的影响

目的 探讨丙泊酚、芬太尼全麻诱导前预注射麻黄素和维库溴铵对维库溴铵的起效时间和诱导后血流动力学的影响.方法 48例全麻下行择期手术的成年患者,ASA分级Ⅰ或Ⅱ级,按随机数余数分组法分成4组,每组12例.在麻醉诱导前预先静注:Ⅰ组麻黄素70μg/kg和0.01 mg/kg维库溴铵、Ⅱ组0.01 mg/kg维库溴铵、Ⅲ组麻...     

Recovery of neuromuscular blockade caused by vecuronium is delayed in patients with hypertriglyceridemia

We investigated the effects of hypertriglyceridemia on the onset and recovery of neuromuscular blockade, induced by vecuronium, over the adductor pollicis muscle, electromyographically. Eighteen adult patients with hypertriglyceridemia (hypertriglyceridemia group) and 18 healthy patients with normal serum triglyceride (control group) were studied. The supramaximal stimulating current for train-of-four (TOF) in the hypertriglyceridemia group was significantly higher than that in the control group (45.7 ± 16.7 vs 31.5 ± 9.8 mA; mean ± SD; P = 0.004). The onset of vecuronium 0.1 mg·kg⁻¹-induced neuromuscular blockade in the hypertriglyceridemia group did not significantly differ from that in the control group (240 ± 60 vs 279 ± 88 s; P = 0.132). Times from vecuronium to the return of T1, T2, T3, and T4 in the hypertriglyceridemia group were significantly longer than those in the control group (31.4 ± 6.2 vs 25.5 ± 6.2 min for T1; P = 0.008). During recovery from neuromuscular blockade, T1/control did not differ between the two groups. However, the TOF ratios (T4/T1) in the hypertriglyceridemia group were significantly lower than those in the control group 80–120 min after vecuronium (P < 0.05). We conclude that, in patients with hypertriglycemidemia, a higher current is needed to elicit supramaximal response of the adductor pollicis muscle, and recovery from vecuronium-induced neuromuscular blockade is delayed.     

Influence of epidural lidocaine injection on vecuronium-induced neuromuscular blockade

BACKGROUND: We investigated vecuronium-induced neuromuscular blockade in patients with continuous epidural lidocaine injection and those without epidural lidocaine. METHODS: Lower thoracic epidural injection of lidocaine was commenced at a rate of 2-3 mg x kg(-1) x h(-1) following its bolus injection (1.5-2 mg x kg(-1)) only in epidural group. Neuromuscular function was monitored by acceleromyographic train-of-four (TOF) responses of the adductor pollicis muscle to ulnar nerve stimulation after induction of general anesthesia. RESULTS: Neuromuscular block was obtained by vecuronium 0.1 mg x kg(-1) as an intubating dose and was maintained 5-10% of baseline first twitch (T 1) of TOF responses by continuous vecuronium administration. The maximum depression of T 1 response and onset time obtained by vecuronium 0.1 mg x kg(-1) were not different between the groups, but mean clinical duration from administration of the first dose to T 1 recovery to 5% of baseline was significantly prolonged in group with epidural lidocaine (49.5 min), compared to that without lidocaine (32.3 min). Furthermore, maintenance dose of vecuronium obtained in the group with epidural lidocaine (0.034 mg x kg(-1) x h(-1)) was significantly smaller than that in the group without lidocaine (0.060 mg x kg(-1) x h(-1)). CONCLUSIONS: Based on our results, we conclude that lidocaine injected continuously into the epidural space potentiates vecuronium-induced neuromuscular block.