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

Effects of ropivacaine dosage on electrophysiologic changes of the sciatic nerve in diabetic rats

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0．5ml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0．5ml的0．9％生理盐水作为对照。在注药前、注药后即刻至15min（每分钟1次）以及注药48h后检测坐骨神经的运动神经传导速度（MNCV）、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4min开始降低，在平均10min变为0；给予0．5％罗哌卡因后，其MNCV、AMP在平均3min开始降低，在平均9min变为0；48h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1min开始降低，在平均7min变为0；给予0．5％罗哌卡因后，其MNCV、AMP在平均1min开始降低，在平均6min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。48h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。

Objective To observe the effects of elinieal routine dosages 0 . 375 % and0.5% ropivaeaine on electrophysiologie changes of the sciatic nerve in diabetic rats. Methods Twelve healthy rats and 12 rats with streptozotoein （STZ） induced diabetic peripheral nettropathy were used and further divided to 2 groups. Both sciatic nerves were exposed under general anesthesia. 0. 5 ml of either 0.375% or 0. 5% ropivaeaine was injected in close proximity to the fight sciatic nerve which was the experimental side. 0.5 ml of 0.9% sodium chloride was injected in close proximity to the left sciatic nerve which served as control. Motor nerve conduction velocity （MNCV）, amplitude （AMP） and latency （LAT） of compound muscle action potential were recorded before injection, at the moment of injection, at one minute intervals for up to 15 minutes and 48 hours after the injection. Results MNCV, AMP and LAT didn ＇ t ehange at all the observed time points of the 0 . 9 % sodium chloride injected control side in either healthy rats or diabetic rats. MNCV and AMP in normal rats injected with 0.375% ropivaeaine began to decrease at average 4 minutes and became zero at 10 minutes, while they began to decrease at average 3 minutes and dropped to zero at average 9 minutes while injected with 0.5% ropivaeaine. These parameters returned to baseline levels after 48 hours. MNCV and AMP in diabetic rats injected with 0.375% ropivaeaine began to decrease at average one minute and became zero at 7 minutes, while they began to decrease at average one minute and dropped to zero at 6 minutes with 0.5 % ropivacaine injection. The time course had statistically significant difference between diabetic and normal rats. I.AT had the same change pattern as MNCV and AMP. After 48 hours, MNCV in 0. 375% ropivacaine diabetic group was not different from baseline value（ P 〈 0.05）, but AMP and LAT were still significantly different from ba^line levels. MNCV, AMP and LAT in 0.5% ropivacaine diabetic group had significant difference comparing to baseline levels and levels of 0.375% ropivacaine diabetic group（ P 〈 0.05）. Conclusion Either 0. 375% or 0.5% ropivacaine may deteriorate the diabetic peripheral nerve injury, the latter being more remarkable.