罗哌卡因神经内注射对大鼠急性坐骨神经损伤后功能恢复的影响

目的 观察罗哌卡因神经内给药对大鼠急性坐骨神经损伤后功能恢复的影响.方法 选择健康成年雄性Wistar大鼠36只,经股骨下方肌间隙暴露坐骨神经,用血管夹压迫2 min制备神经损伤模型.随机分为三组,每组12只,分别注入0.25%罗哌卡因0.2 ml(A组)、1.0%罗哌卡因0.2 ml(B组)或生理盐水0.2 ml(C组).术后1、3、7、14、21、28 d测坐骨神经功能指数(SFI).术后14、28 d每组取6只测坐骨神经传导速度(NCV)及组织形态学观察.结果 三组的神经功能均在术后7 d开始恢复.A、B组术后3、7、14、21 d SFI、术后14、28 d NCV显著低于C组(P＜0.05或P＜0.01).术后28 d神经髓鞘染色提示A、B组恢复较C组滞后.结论 0.25%和1. 0%罗哌卡因神经内注射均明显延长大鼠坐骨神经急性损伤后功能的恢复速度.     

不同浓度丁卡因或罗哌卡因对大鼠臂丛神经的毒性

目的 探讨不同浓度丁卡因和罗哌卡因对大鼠臂从神经的毒性.方法 成年雄性SD大鼠48只,体重410 ～ 430 g,采用随机数字表法,将其随机分为8组(n=6):生理盐水组(NS组)、0.25％、0.50％、1.00％丁卡因组(T1-3组)、0.25％、0.50％、1.00％、2.00％罗哌卡因组(R1-4组).随机选取一侧腋鞘,NS组注射生理盐水1.0 ml,T1-3组分别注射0.25％、0.50％、1.00％丁卡因0.5 ml,R1-3组分别注射0.25％、0.50％、1.00％罗哌卡因1.0 ml,R4组注射2.00％罗哌卡因0.5 ml.另一侧腋鞘作为对照.于注药后5d时检测臂从神经复合动作电位及其传导速度(NCV),并采用光镜和透射电镜观察臂从神经的病理学结果.结果 与对照侧和NS组比较,T2-3组和R3-4组臂丛神经复合动作电位降低,NCV减慢(P＜0.05);T1组、T2组和T3组臂从神经复合动作电位位依次降低,NCV依次减慢(P＜0.05);与R1-3组比较,R4组臂丛神经复合动作电位降低,NCV减慢(P＜0.05).病理学改变:T2组、T3组和R4组神经束膜明显水肿,髓鞘板层分离、断裂、重度脱髓鞘,轴突萎缩;R3组为“脱髓鞘”现象,髓鞘板层分离、断裂、重度脱髓鞘,轴突萎缩.结论 0.50％、1.00％丁卡因和1.00％、2.00％罗哌卡因可导致大鼠臂从神经产生病理性损伤,且损伤程度与其浓度有关.     

利多卡因复合布比卡因或罗哌卡因鞘内注射对大鼠脊髓神经毒性的影响

目的探讨利多卡因复合布比卡因或罗哌卡因鞘内注射对大鼠脊髓神经毒性的影响。方法雄性SD大鼠48只,体重250~300g,随机分为六组:生理盐水组(N组)、1.065%布比卡因组(B组)、1.5%罗哌卡因组(R组)、5%利多卡因组(L组)、5%利多卡因+1.065%布比卡因组(LB组)和5%利多卡因+1.5%罗哌卡因组(LR组),每组8只。麻醉后行鞘内置管手术,于术前1d测定各组大鼠的甩尾潜伏期(TFL)和机械缩足阈值(MWT)作为基础值,再分别于鞘内注药后1、2、3、4d测试各组大鼠的TFL和MWT;分别观察大鼠鞘内注药后10、30min、1、2、3、4h及注药后1、2、3、4d各时点的双后腿运动情况,记录下肢运动恢复时间的变化。术后4d观察完上述指标后处死灌注,取脊髓及马尾组织染色,光镜及透射电镜下观察脊髓的病理改变,并对马尾神经进行病理损伤评分。结果鞘内注药后1~4dLR组TFL明显长于N、L、B、R、LB组(P0.05);L、B、R、LB组与N组TFL差异无统计学意义;六组大鼠各时点MWT差异无统计学意义。六组大鼠鞘内注射后运动恢复时间差异无统计学意义;LR组病理损伤评分明显高于N、L、B、R、LB组。L、B、R、LB组与N组病理损伤评分差异无统计学意义(P0.05)。光镜观察:N、B和R组脊髓结构正常。L和LB组见马尾神经纤维局灶水肿。LR组见马尾神经纤维水肿及脱髓鞘改变,伴尾段脊髓后角白质的水肿。透射电镜:B和R组仅见轻微的有髓神经纤维及无髓神经纤维水肿,L和LB组部分有髓神经纤维出现局灶板层结构疏松,LR组见轴索肿胀、变型、轴索与髓鞘分离,无髓神经纤维轮廓消失。结论 5%利多卡因复合1.5%罗哌卡因鞘内注射后的脊髓神经毒性较其单独注药明显增强,而复合等效浓度的布比卡因后,其脊髓神经毒性变化不明显。     

物理治疗促进坐骨神经损伤再生的实验研究

目的周围神经损伤是临床常见疾病,评估物理治疗对坐骨神经损伤后功能恢复的影响,为临床治疗提供一定参考。方法雌性Wistar大鼠64只,体重252～365g,随机分为A、B、C、D4组,每组16只。各组分离右侧坐骨神经后,B、C、D组钳夹坐骨神经造成损伤模型,A组不进行钳夹作为对照。术后第2天,B组未治疗,C组采用单纯电刺激治疗,D组采用电刺激、分米波和红外线综合治疗。分别于治疗后0、7、14、30d行坐骨神经功能指数(sciatic nerve function index,SFI)、神经传导速度(motor nerve conduction velocity,MNCV)检测,并取材行组织形态学观察和透射电镜观察,取治疗后30d切片行轴突图像分析。结果治疗后0、7d,B、C、D组SFI显著高于A组(P<0.05),B、C、D组间差异无统计学意义(P>0.05);治疗后14、30d,D组SFI显著降低,30d时与A组比较差异无统计学意义(P>0.05),B、C组SFI有所降低,但与A组比较差异仍有统计学意义(P<0.05)。治疗后0、7、14d,B、C、D组MNCV显著低于A组(P<0.05),C、D组与B组比较差异有统计学意义(P<0.05),14d时D组高于C组(P<0.05);治疗后30d,B、C组仍显著低于A组(P<0.05),但D组与A组比较差异无统计学意义(P>0.05)。治疗后0、7d,透射电镜观察各组仅见胶原蛋白和脂质成分;治疗后14、30d,B、C、D组可见大量雪旺细胞和再生神经纤维,D组最显著。治疗30d时轴突图像分析示,D组有髓神经纤维数、轴突直径及髓鞘厚度与A组比较差异均无统计学意义(P<0.05),有髓神经纤维数量和轴突直径显著高于B、C组(P<0.05),髓鞘厚度与C组比较差异无统计学意义(P>0.05)。结论物理治疗有促进大鼠损伤周围神经再生的作用。     

不同浓度的罗哌卡因对糖尿病大鼠坐骨神经电生理的影响

目的 观察临床常用浓度0.375%与0.5%的罗哌卡因对糖尿病大鼠坐骨神经电生理的影响.方法 健康及链脲佐菌素(STZ)糖尿病大鼠各12只,分别随机分为二组.全麻下解剖、暴露双侧坐骨神经,在右侧坐骨神经附近给予0.5 ml的0.375%或0.5%罗哌卡因作为实验,在左侧坐骨神经附近均给予0.5 ml的0.9%生理盐水作为对照.在注药前、注药后即刻至15 min(每分钟1次)以及注药48 h后检测坐骨神经的运动神经传导速度(MNCY)、动作电位波幅(AMP)、潜伏期(LAT).结果 所有健康大鼠及糖尿病大鼠的生理盐水对照组,其MNCV、AMP、LAT在注药前后各观察时点比较均没有变化.健康大鼠给予0.375%罗哌卡因后,其MNCV、 AMP在平均4 min开始降低,在平均10 min变为0;给予0.5%罗哌卡因后,其MNCV、AMP在平均3 min开始降低,在平均9 min变为0;48 h后其MNCV、AMP都恢复到基础值水平.而糖尿病大鼠给予0.375%罗哌卡因后,其MNCV、AMP在平均1 min开始降低,在平均7 min变为0;给予0.5%罗哌卡因后,其MNCV、AMP在平均1 min开始降低,在平均6 min变为0;其变化时间与健康大鼠相比,差异具有统计学意义(P＜0.05).LAT在变化时间上与MNCV、AMP一致.48 h后糖尿病大鼠0.375%罗哌卡因组MNCV较基础值没有明显变化(P＞0.05),但AMP、LAT较基础值有明显变化(P＜0.05);而0.5%罗哌卡因组MNCV、AMP、LAT较基础值及0.375%罗哌卡因组均有明显变化(P＜0.05).结论0.375%与0.5%的罗哌卡因对糖尿病大鼠行坐骨神经阻滞时均可加重其神经损伤,后者更为严重.     

人羊膜上皮细胞对大鼠坐骨神经再生影响的实验研究

目的 通过实验研究了解人羊膜上皮细胞(human amniotic epithelial cells,HAECs)对大鼠坐骨神经再生的促进作用.方法 取60只SD大鼠随机分为两组,羊膜细胞组和对照组,各组再分为2周和4周组,每组15只.制作大鼠周围神经损伤再生室模型,HAECs组局部应用培养的HAECs,对照组局部使用等量的生理盐水.术后分别于2周、4周检测神经传导功能和HE染色观察神经纤维形态学变化.结果 术后2周两组的神经电生理及组织学检测比较差异无统计学意义;4周HAECs组的大鼠坐骨神经传导功能明显恢复,HE染色显示术后坐骨神经手术部位出现大量炎性肉芽组织,呈现纤维性修复,吻合口以远HAECs组神经纤维形态结构较对照组完整,神经纤维与髓鞘直径均较对照组大.结论 HAECs移植可加速大鼠坐骨神经损伤后神经传导功能恢复,有助于有髓神经纤维损伤后的轴突与髓鞘的再生修复.     

人羊膜上皮细胞对大鼠坐骨神经再生影响的实验研究

目的 通过实验研究了解人羊膜上皮细胞(human amniotic epithelial cells,HAECs)对大鼠坐骨神经再生的促进作用.方法 取60只SD大鼠随机分为两组,羊膜细胞组和对照组,各组再分为2周和4周组,每组15只.制作大鼠周围神经损伤再生室模型,HAECs组局部应用培养的HAECs,对照组局部使用等量的生理盐水.术后分别于2周、4周检测神经传导功能和HE染色观察神经纤维形态学变化.结果 术后2周两组的神经电生理及组织学检测比较差异无统计学意义;4周HAECs组的大鼠坐骨神经传导功能明显恢复,HE染色显示术后坐骨神经手术部位出现大量炎性肉芽组织,呈现纤维性修复,吻合口以远HAECs组神经纤维形态结构较对照组完整,神经纤维与髓鞘直径均较对照组大.结论 HAECs移植可加速大鼠坐骨神经损伤后神经传导功能恢复,有助于有髓神经纤维损伤后的轴突与髓鞘的再生修复.     

鞘内注射不同浓度甲磺酸罗哌卡因对大鼠脊髓的神经毒性

目的 评价鞘内注射不同浓度甲磺酸罗哌卡因对大鼠脊髓的神经毒性.方法 取鞘内置管成功的Wistar大鼠60只,体重210～220 g,雌雄不拘,随机分为5组(n=12),对照组(C组)鞘内注射0.9%NaCl溶液0.4 ml;不同浓度甲磺酸罗哌卡因组(R1～4组)鞘内注射甲磺酸罗哌卡因0.4 ml,浓度依次为0.224%、0.447%、0.671%、0.894%.记录阻滞起效时间(鞘内给药结束至鼠尾丧失运动的时间)和维持时间(鼠尾丧失运动至恢复运动的时间).鞘内给药后第7天处死大鼠,取L4.5脊髓节段,透射电镜下观察超微结构,并进行脊髓损伤评分.脊髓损伤评分≥2分为发生神经毒性,记录脊髓神经毒性的发生情况.结果 随甲磺酸罗哌卡因浓度的升高起效时间逐渐缩短,维持时间逐渐延长(P＜0.05或0.01).脊髓神经毒性发生率C组为0,R1组为0,R2组为17%,R3组为42%,R4组为100%;随甲磺酸罗哌卡因浓度的升高,脊髓神经毒性发生率逐渐增加(P＜0.05或0.01).结论 鞘内注射甲磺酸罗哌卡因对大鼠可产生脊髓神经毒性,且取决于其浓度.     

丁卡因和罗哌卡因对大鼠臂丛神经毒性的比较

目的 比较丁卡因和罗哌卡因对大鼠臂丛神经的毒性.方法 成年雄性SD大鼠48只,体重410～430 g,随机分为8组(n=6):NS组、D1-3组和R1-4组.各组大鼠随机选取一侧腋鞘,分别注射生理盐水1ml,0.25%、0.5%、1%丁卡因0.5 ml,0.25%、0.5%、1%罗哌卡因1 ml,2%罗哌卡因0.5 ml.以另一侧作为对照,注射后5 d时,测定臂丛神经动作电位的最大振幅及传导速度(NCV).结果 与对照侧比较,D2,3,组和R3,4组注射侧臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与NS组注射侧比较,D2,3组和R3,4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D1组注射侧比较,D2,3组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D2组注射侧比较,D3组臂丛神经动作电位的最大振幅降低,NCV减慢,R2组臂丛神经动作电位的最大振幅升高,NCV加快(P<0<05);与D1组注射侧比较,R3组臂丛神经动作电位的最大振幅升高,NCV加快(P<0.05);与R1-3组注射侧比较,R4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05).结论 等效剂量丁卡因对臂丛神经的毒性较罗哌卡因大.     

丁卡因和罗哌卡因对大鼠臂丛神经毒性的比较

目的 比较丁卡因和罗哌卡因对大鼠臂丛神经的毒性.方法 成年雄性SD大鼠48只,体重410～430 g,随机分为8组(n=6):NS组、D1-3组和R1-4组.各组大鼠随机选取一侧腋鞘,分别注射生理盐水1ml,0.25%、0.5%、1%丁卡因0.5 ml,0.25%、0.5%、1%罗哌卡因1 ml,2%罗哌卡因0.5 ml.以另一侧作为对照,注射后5 d时,测定臂丛神经动作电位的最大振幅及传导速度(NCV).结果 与对照侧比较,D2,3,组和R3,4组注射侧臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与NS组注射侧比较,D2,3组和R3,4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D1组注射侧比较,D2,3组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D2组注射侧比较,D3组臂丛神经动作电位的最大振幅降低,NCV减慢,R2组臂丛神经动作电位的最大振幅升高,NCV加快(P<0<05);与D1组注射侧比较,R3组臂丛神经动作电位的最大振幅升高,NCV加快(P<0.05);与R1-3组注射侧比较,R4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05).结论 等效剂量丁卡因对臂丛神经的毒性较罗哌卡因大.     

Long-term evaluation of motor function following intraneural injection of ropivacaine using walking track analysis in rats

Background. There is a paucity of data regarding neurologicfunction following nerve injury. Our objective was the long-termevaluation of motor function following intraneural injectionof ropivacaine in rats using the sciatic function index (SFI),derived from walking track analysis. Methods. Rats were randomly assigned to one of four groups of13 animals each. A needle was inserted under magnification intothe left sciatic nerve and 0.2 ml of normal saline, formalin15%, ropivacaine 0.2 or 0.75% were injected intraneurally. Theright side was sham operated. Walking track analysis was performedthe day before and on days 1, 4, 7, 11, 15, 18, 21, and 67 followingintraneural injection. At the end of the experiment (day 67)a semi-quantitative evaluation of neuropathologic changes wasperformed by three independent observers. Results. Animals treated with saline and ropivacaine (0.2 and0.75%) had no detectable impairment of motor function at anytime point. In contrast, rats treated with formalin had a completeloss of motor function immediately after the intraneural injection,which persisted until day 21 and returned to normal by day 67.Important histopathologic changes (score=2) with excellent inter-observeragreement were seen only in the group treated with formalin.This applied to both axonal degeneration and Schwann cell densityevaluations. Conclusions. These findings suggest that intraneural injectionsof ropivacaine at concentrations routinely used in clinicalpractice appear to have no deleterious effect on sciatic nervemotor function in this experimental rat model.     

碱性成纤维细胞生长因子在大鼠坐骨神经损伤修复中的作用

目的　研究碱性成纤维细胞生长因子（ｂ Ｆ Ｇ Ｆ）对周围神经损伤的促修复作用。方法　建立大鼠坐骨神经离断模型,镜下进行神经外膜缝合,局部滴加药物和术后肌注ｂ Ｆ Ｇ Ｆ 以及临床用药神经生长因子（ Ｎ Ｇ Ｆ）,通过神经传导速度和功能指数评定观察坐骨神经修复情况。结果　术后１ 个月,以正常对照为标准,０ 基线为正常水平,生理盐水、 Ｎ Ｇ Ｆ、ｂ Ｆ Ｇ Ｆ 使用组神经功能指数评定结果分别为：－ １１４．３０±１０．３４、－ ７０．５０±１１．０１、－ ５０．４５±７．８２;术后３ 个月,分别为：－ ５４．９６±１６．４６、－ ３５．２１±１０．８０、－ ２７．５３±１１．２３,ｂ Ｆ Ｇ Ｆ组神经传导速度明显快于生理盐水组和 Ｎ Ｇ Ｆ 组（ Ｐ＜ ０．０１）。结论　ｂ Ｆ Ｇ Ｆ对坐骨神经损伤具有显著的促功能修复作用,并且在神经损伤早期就能最有效地发挥作用,效果明显优于临床用药 Ｎ Ｇ Ｆ。     

Intraneural hematoma with extrinsic compression: experimental study in rats and therapeutic options

Intraneural hematoma can result in the median nerve in the carpal tunnel after trauma or coagulation disorders. The decision for expectant management or decompressive surgical techniques is still controversial. Fifty male Wistar rats were divided into five groups. The sciatic nerve was wrapped around with a silastic device in four groups. In group A, the sciatic nerve was just wrapped by the silastic tube. In group B, an intraneural injection of autologous blood was added. In group C, after the hematoma creation, the silastic device was removed and a longitudinal epineurotomy was performed. In group D, the silastic device was removed after the hematoma, but the nerve was not opened. In group E (sham-operated), the sciatic nerve was exposed without hematoma or compression. Nerve function recovery was assessed periodically over 61 days using the Bain-Mackinnon-Hunter Sciatic Function Index (SFI). Group A (extrinsic compression) presented initial SFI of -26.29 +/- 2.89, with return to baseline values on the fifth postoperative day. Group B (hematoma and extrinsic compression) exhibited the poorest function (SFI of -85.23 +/- 3.51) after surgery and recovery in 23 days. Group C (liberation of silastic and hematoma drainage through epineurotomy) and group D (only removal of the silastic tube) presented similar initial SFI values of -32.78 +/- 7.45 and -45.13 +/- 6.84, respectively. In both the groups, the SFI values returned to baseline level on fifth postoperative day. The statistical analysis of SFI identified a significant difference (P < .0001) between the expectant management (group B) and the descompressive surgery approach (groups C and D) by 1st to 19th postoperative day. The number of degenerative fibers and density of degenerative fibers were statistically significantly longer in group B when compared with the other groups. There was no statistical difference between the other groups when these parameters were analyzed. Thus, immediate decompressive procedures of the intraneural hematoma provide a faster functional recovery and reduce the damage to the axon fibers.     

Neurologic and histologic outcome after intraneural injections of lidocaine in canine sciatic nerves

BACKGROUND: Inadvertent intraneural injection of local anesthetics may result in neurologic injury. We hypothesized that an intraneural injection may be associated with higher injection pressures and an increase in the risk of neurologic injury. METHODS: The study was conducted in accordance with the principles of laboratory animal care, and was approved by the Laboratory Animal Care and Use Committee. Fifteen dogs of mixed breed (16-21 kg) were studied. After general endotracheal anesthesia, the sciatic nerves (n= 30) were exposed bilaterally. Under direct vision, a 25-gauge, long-beveled needle (30 degrees) was placed either epineurally (n= 10) or intraneurally (n= 20), and 4 ml of preservative-free lidocaine 20 mg/ml was injected using an automated infusion pump (4 ml/min). Injection pressure data were acquired using an in-line manometer coupled to a computer via an analog-to-digital conversion board. After injection, the animals were awakened and subjected to serial neurologic examinations. One week later, the dogs were killed, the sciatic nerves excised and histologic examination was performed by pathologists blind to the purpose of the study. RESULTS: All perineural injections resulted in low pressures (< or = 5 psi). In contrast, eight of 20 intraneural injections resulted in high pressures (20-38 psi) at the beginning of the injection. Twelve intraneural injections, however, resulted in pressures of less than 12 psi. Neurologic function returned to baseline within 3 h after perineural injections and within 24 h after intraneural injections, when the measured injection pressures were less than 12 psi. Neurologic deficits persisted throughout the study period after all eight intraneural injections that resulted in high injection pressures. Histologic examination of the affected nerves revealed fascicular axonolysis and cellular infiltration. CONCLUSIONS: The data in our canine model of intraneural injection suggest that intraneural injections do not always lead to nerve injury. High injection pressures during intraneural injection may be indicative of intrafascicular injection and may predict the development of neurologic injury.     

丁卡因和罗哌卡因对大鼠臂丛神经毒性的比较

目的 比较丁卡因和罗哌卡因对大鼠臂丛神经的毒性.方法 成年雄性SD大鼠48只,体重410～430 g,随机分为8组(n=6):NS组、D1-3组和R1-4组.各组大鼠随机选取一侧腋鞘,分别注射生理盐水1ml,0.25%、0.5%、1%丁卡因0.5 ml,0.25%、0.5%、1%罗哌卡因1 ml,2%罗哌卡因0.5 ml.以另一侧作为对照,注射后5 d时,测定臂丛神经动作电位的最大振幅及传导速度(NCV).结果 与对照侧比较,D2,3,组和R3,4组注射侧臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与NS组注射侧比较,D2,3组和R3,4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D1组注射侧比较,D2,3组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D2组注射侧比较,D3组臂丛神经动作电位的最大振幅降低,NCV减慢,R2组臂丛神经动作电位的最大振幅升高,NCV加快(P<0<05);与D1组注射侧比较,R3组臂丛神经动作电位的最大振幅升高,NCV加快(P<0.05);与R1-3组注射侧比较,R4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05).结论 等效剂量丁卡因对臂丛神经的毒性较罗哌卡因大.     

丁卡因和罗哌卡因对大鼠臂丛神经毒性的比较

目的 比较丁卡因和罗哌卡因对大鼠臂丛神经的毒性.方法 成年雄性SD大鼠48只,体重410～430 g,随机分为8组(n=6):NS组、D1-3组和R1-4组.各组大鼠随机选取一侧腋鞘,分别注射生理盐水1ml,0.25%、0.5%、1%丁卡因0.5 ml,0.25%、0.5%、1%罗哌卡因1 ml,2%罗哌卡因0.5 ml.以另一侧作为对照,注射后5 d时,测定臂丛神经动作电位的最大振幅及传导速度(NCV).结果 与对照侧比较,D2,3,组和R3,4组注射侧臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与NS组注射侧比较,D2,3组和R3,4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D1组注射侧比较,D2,3组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D2组注射侧比较,D3组臂丛神经动作电位的最大振幅降低,NCV减慢,R2组臂丛神经动作电位的最大振幅升高,NCV加快(P<0<05);与D1组注射侧比较,R3组臂丛神经动作电位的最大振幅升高,NCV加快(P<0.05);与R1-3组注射侧比较,R4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05).结论 等效剂量丁卡因对臂丛神经的毒性较罗哌卡因大.     

丁卡因和罗哌卡因对大鼠臂丛神经毒性的比较

目的 比较丁卡因和罗哌卡因对大鼠臂丛神经的毒性.方法 成年雄性SD大鼠48只,体重410～430 g,随机分为8组(n=6):NS组、D1-3组和R1-4组.各组大鼠随机选取一侧腋鞘,分别注射生理盐水1ml,0.25%、0.5%、1%丁卡因0.5 ml,0.25%、0.5%、1%罗哌卡因1 ml,2%罗哌卡因0.5 ml.以另一侧作为对照,注射后5 d时,测定臂丛神经动作电位的最大振幅及传导速度(NCV).结果 与对照侧比较,D2,3,组和R3,4组注射侧臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与NS组注射侧比较,D2,3组和R3,4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D1组注射侧比较,D2,3组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D2组注射侧比较,D3组臂丛神经动作电位的最大振幅降低,NCV减慢,R2组臂丛神经动作电位的最大振幅升高,NCV加快(P<0<05);与D1组注射侧比较,R3组臂丛神经动作电位的最大振幅升高,NCV加快(P<0.05);与R1-3组注射侧比较,R4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05).结论 等效剂量丁卡因对臂丛神经的毒性较罗哌卡因大.     

丁卡因和罗哌卡因对大鼠臂丛神经毒性的比较

目的 比较丁卡因和罗哌卡因对大鼠臂丛神经的毒性.方法 成年雄性SD大鼠48只,体重410～430 g,随机分为8组(n=6):NS组、D1-3组和R1-4组.各组大鼠随机选取一侧腋鞘,分别注射生理盐水1ml,0.25%、0.5%、1%丁卡因0.5 ml,0.25%、0.5%、1%罗哌卡因1 ml,2%罗哌卡因0.5 ml.以另一侧作为对照,注射后5 d时,测定臂丛神经动作电位的最大振幅及传导速度(NCV).结果 与对照侧比较,D2,3,组和R3,4组注射侧臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与NS组注射侧比较,D2,3组和R3,4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D1组注射侧比较,D2,3组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05);与D2组注射侧比较,D3组臂丛神经动作电位的最大振幅降低,NCV减慢,R2组臂丛神经动作电位的最大振幅升高,NCV加快(P<0<05);与D1组注射侧比较,R3组臂丛神经动作电位的最大振幅升高,NCV加快(P<0.05);与R1-3组注射侧比较,R4组臂丛神经动作电位的最大振幅降低,NCV减慢(P<0.05).结论 等效剂量丁卡因对臂丛神经的毒性较罗哌卡因大.