罗哌卡因硬膜外麻醉用于妇科手术临床观察

目的:观察同等浓度罗哌卡因与布比卡因硬膜外阻滞麻醉用于妇科手术的临床效果。方法:选择ASAⅠ~Ⅱ级择期行子宫次全切除术患者60例,随机分为布比卡因组(n=30)和罗哌卡因组(n=30);硬膜外隙注入试验量1.33%利多卡因3ml后,分别再小剂量(3ml)分次注入0.75%布比卡因或0.75%罗哌卡因至要求麻醉平面。分别观察感觉阻滞平面及下肢运动阻滞的起效时间和维持时间,以及镇痛效果、手术时间、用药总剂量及不良反应。结果:罗哌卡因较布比卡因感觉神经阻滞起效快,运动神经阻滞则起效缓慢、维持时间短及下肢运动阻滞强度弱,术中不良反应发生率低。结论:罗哌卡因麻醉应用于妇科手术,具有良好的临床应用前景。     

小剂量布比卡因腰-硬联合麻醉用于高龄患者股骨颈骨折手术可行性探讨

目的:探讨小剂量布比卡因腰-硬联合麻醉用于用于高龄患者股骨颈骨折手术的可行性。方法:选择ASAⅡ~Ⅲ级高龄患者择期股骨颈骨折手术患者58例,采用0.75%布比卡因6mg腰-硬联合麻醉后,观察麻醉前、麻醉后5min、麻醉后15min、麻醉后30min、收缩血压(SBP)、舒张血压(DBP)、心率(HR)、血氧饱和度(SpO2)血流动力学变化、术中呼吸、,手术中的麻醉效果、麻醉后并发症的影响。结果:术前、术中血流动力学、呼吸无明显改变(P0.05)。结论:小剂量布比卡因腰-硬联合麻醉应用于高龄患者股骨颈骨折手术麻醉中,对呼吸、循环系统影响轻微,具有麻醉效果确切、安全可靠、不良反应小等优点。     

罗哌卡因联合舒芬太尼在剖宫产术后镇痛中的临床效果分析

目的：探讨罗哌卡因联合舒芬太尼在剖宫产术后镇痛中的临床疗效。方法方便选取2014年3月—2015年3月该院麻醉科收诊的剖宫产产妇60例,随机法分为观察组及对照组各30例,对照组术后给予罗哌卡因联合吗啡镇痛治疗,观察组术后给予罗哌卡因联合舒芬太尼镇痛治疗,记录并分析两组产妇镇痛效果。结果观察组术后2h、8h、12 h、24 hVAS评分分别为(1.98±0.81)分、(2.28±0.78)分、(1.66±0.67)分、(1.17±0.61)分,均低于对照组(3.51±1.07)分、(3.82±1.03)分、(3.24±0.95)分、(2.16±0.55)分,且差异具有统计学意义(P<0.05)；观察组术后肌力恢复正常时间和肛门排气时间分别为(7.28±1.16)h、18.49±1.71)h,均低于对照组(15.67±3.59)h、20.84±2.10)h,且差异有统计学意义(P<0.05)；③观察组产妇术后不良反应发生率为6.67%,显著低于对照组26.67%,且差异具有统计学意义(P<0.05)；结论罗哌卡因联合舒芬太尼在剖宫产术后镇痛中的效果优于罗哌卡因联合吗啡,不良反应低,能有效缓解孕妇术后疼痛。     

左旋布比卡因腰麻用于剖宫产术的临床观察

我科白2005年8月至2006年4月应用0．75％左旋布比卡因腰麻行剖宫产手术30例，效果良好，报道如下。     

罗哌卡因联合芬太尼与布比卡因在腰—硬联合麻醉中用于剖宫产术的比较

目的:探讨罗哌卡因联合芬太尼腰—硬联合麻醉用于剖宫产术的优越性。方法:通过罗哌卡因联合芬太尼与布比卡因在腰—硬联合麻醉中对照,观察在麻醉效果、血流动力学等不良反应及术后恢复等方面的差别。结果:应用罗哌卡因联合芬太尼用于剖宫产术麻醉效果确切,对循环影响小,不良反应少,术后恢复快。结论:罗哌卡因联合芬太尼腰—硬联合麻醉用于剖宫产术效果满意,利于术后恢复。     

不同剂量布比卡因联合麻醉用于剖宫产术对母婴肾素-血管紧张素-醛固酮系统的影响

目的:比较不同剂量布比卡因腰麻-硬膜外联合麻醉(CSEA)用于产科麻醉的效果和安全性,探讨最佳的方法和药物剂量。方法:ASAI-Ⅱ级初产妇60例于腰麻-硬膜外联合麻醉下行剖宫产手术,随机双盲分为3组,Ⅰ组(n=20)腰麻用药为0·75%布比卡因1ml(7·5mg),Ⅱ组(n=20)腰麻用药为0·75%布比卡因0·7ml(5·25mg),Ⅲ组(n=20)腰麻用药为0·75%布比卡因1ml(7·5mg),但在给药麻的同时静脉滴注麻黄碱30mg。术中如有麻醉效应不足时经硬膜导管补充2%利多卡因,术中连续监测呼吸和循环状况,同时分别于注射局麻(T0),切皮后即刻(T1),胎儿娩出后即刻(T2),术毕即刻(T3),取母体静脉血和胎儿娩出后脐动、静脉血测定血清肾素活性(PRA),血管肾张素(AT-Ⅱ)和醛固酮(ALD)浓度,评估麻醉效应,并观察围术期不良反应的发生及新生儿情况。结果:术中Ⅰ组血压波动较大,恶心呕吐出现的较多,多出现给药后10min以内。T2,T3的PRA,AT-Ⅱ,ALD值均比T0,T1值明显降低(P<0·01)。Ⅱ,Ⅲ组血压较稳定,恶心呕吐少见,T1,T2,T3的PRA,AT-Ⅱ,ALD值均比T0值明显降低,胎儿脐动、静脉血中三者值差异不明显,但明显低于母体T0值。结论:CSEA用于宫产手术时,只要运用得当是安全有效的方法,不会对母体RAAS产生不良影响。     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.