共查询到19条相似文献,搜索用时 171 毫秒
1.
罗库溴铵、维库溴铵和阿曲库铵用于全麻气管插管肌松效应的对比研究 总被引:6,自引:0,他引:6
目的观察比较罗库溴铵、维库溴铵及阿曲库铵在全麻诱导气管插管时的肌松效应及不良反应。方法ASAⅠ~Ⅱ级择期全麻下行腹腔镜胆囊切除手术患者120例,随机分为:罗库溴铵组(Ⅰ组)、维库溴铵组(Ⅱ组)、阿曲库铵组(Ⅲ组),每组给2倍ED95剂量肌松剂。Ⅰ组按用量再分为:Ⅰa组(2倍ED95,0.6 mg/kg)、Ⅰb组(3倍ED95,0.9 mg/kg)2个亚组。每组各30例。麻醉诱导依次静注咪达唑仑0.06 mg/kg、芬太尼4μg/kg,异丙酚2 mg/kg后,Ⅰa、Ⅰb组分别静注罗库溴铵0.6 mg/kg、罗库溴铵0.9 mg/kg,Ⅱ组静注维库溴铵0.15 mg/kg,Ⅲ组静注阿曲库铵0.5 mg/kg。观察各组气管插管时的肌松效果及不良反应。结果Ⅰ组的起效时间及插管状态优良率均明显高于Ⅱ、Ⅲ组,Ⅰb组的插管条件好于Ⅰa组。Ⅰ组的支气管痉挛、皮疹等不良反应的发生率明显低于其他组,对循环系统的影响也较小。结论罗库溴铵比维库溴铵、阿曲库铵起效快,恢复迅速,不良反应少,是较好的全麻气管插管肌松药。 相似文献
2.
比较性观察阿曲库铵和维库溴铵量-效关系和恢复时相特征。选择60例ASAI级,年龄17~50岁,施择期整形外科手术的中国患者,分层随机平均分成阿曲库铰组和维库溴铵组。用60%NO2-O2-硫喷妥钠-芬太尼维持麻醉。用加速度仪监测神经肌肉功能,采用TOF刺激方式,以T1抑制的百分比为研究指标。用累计给药方法建立阿曲库铵和维库溴铵的量-效关系曲线。根据用最小二乘法建立的量-效关系曲线,阿曲库铵的神经肌肉阻滞作用强度仅为维库溴铵的17%。两药的ED50、ED90和ED95均有明显差别。应用等效剂量(1.5×ED95)后,两药的高峰时间、临床肌松时间、恢复时间和体内作用时间均无明显差别。结论:阿曲库铵是一弱效能的肌松药,而维库溴接为一强效能肌松药。阿曲库按和维库溴铵的作用强度比率为1/6。应用等效剂量后,两药的恢复时相无明显差别。 相似文献
3.
目的:研究罗库溴铵对追加的维库溴铵肌松效应的影响及罗库溴铵-维库溴铵先后给药法的临床价值。方法:观察2倍ED95剂量的罗库溴铵(0.6mg.kg^-1)、维库溴铵(0.1mg.kg^-1)分别诱导时的时效及插管条件,以及插管后对追加的1倍ED95剂量的维库溴铵的起效及维持时间的影响。结果:罗库溴铵阻滞起效时间显著快于维库溴铵(P〈0.01),二者产生的插管条件及维持时间相似;罗库溴铵插管后对追加的 相似文献
4.
目的 探讨顺苯磺酸阿曲库铵和维库溴铵在静吸复合麻醉诱导起效及麻醉维持时间的比.方法 选择3~80岁Ⅰ~Ⅱ级美国麻醉医师协会(ASA)级患者50例随机分为(A组)顺苯磺酸阿曲库铵组(B组)维库溴铵组.每组各25例,以芬太尼和丙泊酚及咪达唑仑诱导及维持,观察患者肌肉松弛起效及完善插管时间和肌松恢复时间.结果 顺苯磺酸阿曲库铵起效时间稍慢,肌松恢复时间较维库溴铵短.结论 顺苯磺酸阿曲库铵在全麻诱导起效时间较维库溴铵稍慢,维持肌松时效短,而且不经肝肾代谢,更适合于短小手术及肝肾功能障碍患者. 相似文献
5.
目的:比较罗库溴铵和维库溴铵对风心病二尖瓣狭窄患者的临床药效及气管插管的效果,以及对心血管功能的影响。方法:选择40例体外循环下行二尖瓣置换术的患者,随机分为二组(n=20),分别给予罗库溴铵0.6mg/kg和维库溴铵0.1mg/kg。分别记录气管插管时间、心率、收缩压、舒张压和平均动脉压及ST段的变化,从上下颌、声带、膈肌、肢动来判断气管插管效果。结论:罗库溴铵0.6mg/kg可安全地应用于二尖瓣置换术患者,无心肌缺血改变。罗库溴铵和维库溴铵对心血管无显著影响的非去极化肌松药。 相似文献
6.
目的:研究罗库溴铵对追加的维库溴铵肌松效应的影响及罗库溴铵维库溴铵先后给药法的临床价值。方法:观察2倍ED95剂量的罗库溴铵(0.6mg·kg-1)、维库溴铵(0.1mg·kg-1)分别诱导时的时效及插管条件,以及插管后对追加的1倍ED95剂量的维库溴铵的起效及维持时间的影响。结果:罗库溴铵阻滞起效时间显著快于维库溴铵(P<0.01),二者产生的插管条件及维持时间相似;罗库溴铵插管后对追加的维库溴铵药效无影响。结论:罗库溴铵维库溴铵先后给药法合理安全,有重要临床价值。 相似文献
7.
张月梅 《临床合理用药杂志》2015,(18)
目的:比较维库溴铵与顺式阿曲库铵苯磺酸盐(顺式阿曲库铵)在胆囊切除术中的肌松效果。方法选取2011年10月—2014年10月孝义市人民医院收治的胆囊结石患者160例,随机分为维库溴铵组与顺式阿曲库铵组,各80例。维库溴铵组患者静脉注射维库溴铵,顺式阿曲库铵组静脉注射顺式阿曲库铵。观察两组患者肌松药起效时间、临床作用时间、肌肉松弛恢复时间及气管插管等级评估情况。结果顺式阿曲库铵组患者肌松药起效时间及肌肉松弛恢复时间短于维库溴铵组,临床作用时间长于维库溴铵组,差异有统计学意义( P ﹤0.05);顺式阿曲库铵组患者气管插管良好率高于维库溴铵组,差异有统计学意义( P ﹤0.05)。结论顺式阿曲库铵在胆囊切除术中的肌松效果优于维库溴铵,药物起效时间短,作用时间长,气管插管等级评估高,易操作。 相似文献
8.
目的探讨罗库溴铵、维库溴铵、阿曲库铵及自身预注对顺式阿曲库铵起效时间和插管条件的影响。方法选取自2008年2月~2011年2月来我院接受全麻并择期手术的患者100例,随机分为Ⅰ~Ⅴ5个组,每组20例。Ⅴ组静脉注射生理盐水1mL,Ⅰ~Ⅳ组分别注射罗库溴铵0.06mg·kg-1、维库溴铵0.01mg·kg-1、阿曲库铵0.05mg·kg-1、顺式阿曲库铵0.01mg·kg-1。3min后Ⅴ组静脉注射顺式阿曲库铵0.1mg·kg-1,Ⅰ~Ⅳ组静脉注射顺式阿曲库铵0.14mg·kg-1。结果Ⅴ组的起效时间显著较Ⅰ~Ⅳ组长(P<0.05),Ⅳ组的起效时间长于其他3组(P<0.05),Ⅰ~Ⅲ组间比较无显著性差异(P>0.05);Ⅴ组的插管条件明显低于Ⅰ~Ⅳ组(P<0.05)。结论罗库溴铵、维库溴铵、阿曲库铵预注及自身预注均能有效缩短顺式阿曲库铵的起效时间,改善插管条件,是临床采用顺式阿曲库铵进行快速诱导插管的行之有效的方法。 相似文献
9.
目的:探讨维库溴铵和阿曲库铵非去极化肌松药不同阻滞深度对择期手术患者的影响。方法选取2011年5月-2013年5月间于本院行择期手术治疗的患者54例,按其手术治疗顺序进行编号并随机分为对照组(27例)和观察组(27例),对照组患者麻醉应用维库溴铵肌松药,观察组患者麻醉应用阿曲库铵肌松药,术后均进行新斯的明拮抗。结果观察组患者肌松药用量明显高于对照组,组间差异具有统计学意义(P〈0.05);两组患者新斯的明用量、停药-拮抗时间、TR值至0.75时间、不同阻滞程度比例等指标差异无统计学意义,患者拮抗前、后血压、心率差异无统计学意义(P〉0.05)。结论维库溴铵和阿曲库铵肌松效果类似,新斯的明术后拮抗肌松效果优,安全性更高。 相似文献
10.
目的:比较罗库溴铵与维库溴铵在全麻诱导后气管插管时的起效时间、肌松程度、插管条件及其组胺释放情况。方法:将合格受试的患者80例,随机分为两组,每组40例,均于静脉注射异丙酚2mg/kg和芬太尼0.3!g/kg,同时予纯氧面罩吸入120秒钟后,在前臂静脉10秒内分别快速注射肌松药。治疗组肌松药给罗库溴铵0.9mg/kg,对照组给维库溴铵0.15mg/kg,行气管插管。用4个成串(TOF)刺激(频率2Hz,串间间隔15秒)通过尺神经,用拇内收肌收缩束判断肌松效应,以T1颤搐值(%)作为判断肌松效应的指标,待T1稳定100%后开始给药观察。并且评估插管条件、组胺释放情况以及循环功能变化。结果:观察组和对照组的起效时间分别为(1.61±0.67)分钟、(3.62±0.95)分钟,两组比较差异有显著性(P<0.01)。而在临床作用时间,以及恢复指数上,两组比较差异无显著性(P>0.05);观察组插管条件优秀31例,良好7例,满意率为97.5%,总有效率为100%;对照组优秀29例,良好8例,满意率为92.5%,总有效率为97.5%。两组插管条件比较差异无显著性(P>0.05);两组病人均未出现支气管痉挛和皮疹情况。结论:罗库溴铵起效时间优于维库溴铵,而在临床作用时间、恢复指数、插管条件与维库溴铵相似,两组均无明显心血管不良反应。罗库溴铵是快速诱导气管插管时的良好肌松药。 相似文献
11.
目的 通过重组受体,观察丙泊酚对胎儿型乙酰胆碱受体和神经型α7乙酰胆碱受体的作用。方法 通过脂质体转染法在HEK293细胞表达胎儿型和α7乙酰胆碱受体。分别研究不同浓度丙泊酚对两种受体亚型的作用。结果 临床相关浓度丙泊酚对100μmol/l乙酰胆碱激发胎儿型和α7乙酰胆碱受体的电流均有抑制作用。不同浓度丙泊酚对胎儿型和α7乙酰胆碱受体电流抑制大小无统计学差异(P>0.05)。相同浓度丙泊酚对胎儿型乙酰胆碱受体抑制大于对α7乙酰胆碱受体的抑制(P<0.05)。结论 从乙酰胆碱受体水平研丙泊酚的作用,结果证明丙泊酚对γ-nAChR和a7-nAChR都有抑制作用,抑制程度与丙泊酚的浓度无关。 相似文献
12.
七氟醚和异氟醚对不同浓度罗库溴铵抑制乙酰胆碱受体内向电流的影响 总被引:1,自引:0,他引:1
目的探讨挥发性麻醉药七氟醚(sevoflurane)、异氟醚(isoflurane)对不同浓度罗库溴铵(rocuronium)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。拟合七氟醚、异氟醚、罗库溴铵抑制受体的浓度效应关系(IC50)。用0.5IC50浓度的七氟醚、异氟醚预处理ε-nAChR,记录浓度为IC5、0.5 IC50、IC50的罗库溴铵对ACh诱发峰电流的抑制率。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-1、(1031.53±62.91)μmol.L-1、(150.45±12.5)μmol.L-1(P<0.01)。0.5 IC50浓度的异氟醚增强IC5浓度罗库溴铵拮抗受体的作用强于七氟醚(P<0.01)。结论七氟醚、异氟醚增强罗库溴铵对ε-nAChR的阻滞作用;两种吸入麻醉药对低浓度的罗库溴铵具有更明显的协同效应,且异氟醚作用强于七氟醚。 相似文献
13.
Aim:
To test the hypothesis that different magnitude of resistance of denervated skeletal muscle to nondepolarizing muscle relaxants (NDMRs) is related to their varying potencies at ɛ-AChR and γ-AChR.Methods:
Both innervated and denervated mouse muscle cells, and human embryonic kidney 293 (HEK293) cells expressing ɛ-AChR or γ-AChR were used. The effects of NDMRs on nAChR were explored using whole-cell patch clamp technique.Results:
NDMRs vecuronium (VEC), atracurium (ATR) and rocuronium (ROC) produced reversible, dose-dependent inhibition on the currents induced by 30 μmol/L acetylcholine both in innervated and denervated skeletal muscle cells. Compared to those obtained in innervated skeletal muscle cells, denervation shifted the concentration-response curves rightward and significantly increased the 50% inhibitory concentration (IC50) values (VEC: from 11.2 to 39.2 nmol/L, P<0.01; ATR: from 24.4 to 129.0 nmol/L, P<0.01; ROC: from 37.9 to 101.4 nmol/L, P<0.01). In HEK293 cell expression system, ATR was less potent at γ-AChR than ɛ-AChR (IC50 values: 35.9 vs 22.3 nmol/L, P<0.01), VEC was equipotent at both receptor subtypes (IC50 values: 9.9 vs 10.2 nmol/L, P>0.05), while ROC was more potent at γ-AChR than ɛ-AChR (IC50 values: 22.3 vs 33.5 nmol/L, P<0.05).Conclusion:
Magnitude differences of resistance to different NDMRs caused by denervation are associated with distinct potencies of NDMRs at nAChR subtypes. 相似文献14.
Aim:
To investigate the effect of magnesium sulfate and its interaction with the non-depolarizing muscle relaxant vecuronium at adult muscle-type acetylcholine receptors in vitro.Methods:
Adult muscle-type acetylcholine receptors were expressed in HEK293 cells. Drug-containing solution was applied via a gravity-driven perfusion system. The inward currents were activated by brief application of acetylcholine (ACh), and recorded using whole-cell voltage-clamp technique.Results:
Magnesium sulfate (1–100 mmol/L) inhibited the inward currents induced ACh (10 μmol/L) in a concentration-dependent manner (IC50=29.2 mmol/L). The inhibition of magnesium sulfate was non-competitive. In contrast, vecuronium produced a potent inhibition on the adult muscle-type acetylcholine receptor (IC50=8.7 nmol/L) by competitive antagonism. Magnesium sulfate at the concentrations of 1, 3, and 6 mmol/L markedly enhanced the inhibition of vecuronium (10 nmol/L) on adult muscle-type acetylcholine receptors.Conclusion:
Clinical enhancement of vecuronium-induced muscle relaxation by magnesium sulfate can be attributed partly to synergism between magnesium sulfate and non-depolarizing muscle relaxants at adult muscle-type acetylcholine receptors. 相似文献15.
目的 利用受体克隆技术 ,建立骨骼肌细胞乙酰胆碱受体 (m nAChR)的实验模型 ,以便进行各种药理研究。方法 应用分子生物学技术将编码小鼠m nAChR的α、β、γ、δ、ε亚基之cDNA分别重组于真核细胞表达质粒pcDNA3 1+ 上 ,用脂质体转染技术 ,将重组后的pcDNA3 1+ 导入HEK2 93细胞 ,使其细胞膜上表达胚胎型乙酰胆碱受体 (γ nAChR)和成年型乙酰胆碱受体 (ε nAChR) ,这样建立了两种m nAChR亚型的实验模型。应用全细胞膜片钳技术测量转染细胞对该受体的内生配基乙酰胆碱的反应。结果 乙酰胆碱可激发转染细胞产生一内向电流 ,电流的大小与乙酰胆碱呈浓度依赖性。结论 HEK2 93细胞在转染后 2 4~ 72h内 ,其细胞膜上表达γ nAChR或ε nAChR ,用于进行各种药理实验。 相似文献
16.
Isobolographic analysis of non-depolarising muscle relaxant interactions at their receptor site 总被引:5,自引:0,他引:5
Administration of certain combinations of non-depolarising muscle relaxants produces greater than expected neuromuscular blockade. Synergistic effects may be explained by drug interactions with the postsynaptic muscle nicotinic acetylcholine receptor. To investigate this hypothesis, the adult mouse muscle nicotinic acetylcholine receptor (alpha(2)beta delta epsilon) was heterologously expressed in Xenopus laevis oocytes and activated by the application of acetylcholine (10 microM). The effects of five individually applied muscle relaxants and six combinations of structurally similar and dissimilar compounds were studied. Drug combinations containing equipotent concentrations of two agents were tested and dose-response curves were determined. All compounds tested alone and in combination produced rapid and readily reversible, concentration-dependent inhibition. Isobolographic and fractional analyses indicated additive interactions for all six tested combinations. These findings suggest that synergistic neuromuscular blocking effects, observed for the administration of certain combinations of muscle relaxants, do not result from purely postsynaptic binding events at the muscle nicotinic acetylcholine receptor, but rather from differential actions on pre- and postsynaptic sites. 相似文献
17.
Jonsson M Wyon N Lindahl SG Fredholm BB Eriksson LI 《European journal of pharmacology》2004,497(2):173-180
Neuromuscular blocking agents predominantly block muscle type nicotinic acetylcholine receptors as opposed to the neuronal type. However, there is growing evidence that neuromuscular blocking agents have affinity to some neuronal nicotinic acetylcholine receptors. The carotid body chemoreceptor as the essential oxygen-sensing cell, relies on cholinergic signalling. Atracurium and vecuronium impair carotid body chemoreceptor activity during hypoxia. Here, we characterize atracurium and vecuronium as antagonists at nicotinic receptors of the carotid body chemoreceptor. Isolated rabbit carotid body preparations with carotid sinus nerve were used, and chemoreceptor activities were recorded. There was a concentration-dependent reduction in the chemoreceptor responses to nicotine, with an IC(50) to 50 microg nicotine of 3.64 and 1.64 microM and to 500 microg nicotine of 27.00 microM and 7.29 microM for atracurium and vecuronium, respectively. It is concluded that atracurium and vecuronium depress nicotine-induced chemoreceptor responses of the carotid body in a dose-dependent fashion. 相似文献
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The muscle-type nicotinic acetylcholine receptor has two nonidentical binding sites for ligands. The selectivity of acetylcholine and the competitive antagonists (+)-tubocurarine and metocurine for adult mouse receptors is known. Here, we examine the site selectivity for four other competitive antagonists: cisatracurium, pancuronium, vecuronium, and rocuronium. We rapidly applied acetylcholine to outside-out patches from transfected BOSC23 cells and measured macroscopic currents. We have reported the IC(50) of the antagonists individually in prior publications. Here, we determined inhibition by pairs of competitive antagonists. At least one antagonist was present at a concentration producing > or =67% receptor inhibition. Metocurine shifted the apparent IC(50) of (+)-tubocurarine in quantitative agreement with complete competitive antagonism. The same was observed for pancuronium competing with vecuronium. However, pancuronium and vecuronium each shifted the apparent IC(50) of (+)-tubocurarine less than expected for complete competition but more than expected for independent binding. The situation was similar for cisatracurium and (+)-tubocurarine or metocurine. Cisatracurium did not shift the apparent IC(50) of pancuronium or vecuronium, indicating independent binding of these two pairs. The data were fit to a two-site, two-antagonist model to determine the antagonist binding constants for each site, L(alphaepsilon) and L(alphadelta). We found L(alphaepsilon)/L(alphadelta) = 0.22 (range, 0.14-0.34), 20 (9-29), 21 (4-36), and 1.5 (0.3-2.9) for cisatracurium, pancuronium, vecuronium, and rocuronium, respectively. The wide range of L(alphaepsilon)/L(alphadelta) for some antagonists may reflect experimental uncertainties in the low affinity site, relatively poor selectivity (rocuronium), or possibly that the binding of an antagonist at one site affects the affinity of the second site. 相似文献