Neurotoxicity of intrathecally administered bupivacaine involves the posterior roots/posterior white matter and is milder than lidocaine in rats
Neurotoxicity of intrathecally administered bupivacaine involves the posterior roots/posterior white matter and is milder than lidocaine in rats
复制标题
DOI：
10.1016/j.rapm.2005.05.005
复制
发表时间：
2005-09-01
影响因子：
5.1
通讯作者：
Hoka, S
中科院分区：
文献类型：
--
作者：
Takenami, T;Yagishita, S;Hoka, S
背景和目的：临床和实验室研究表明利多卡因的神经毒性比布比卡因大。然而，其相对神经毒性的组织学证据很少。因此，我们的病理和功能比较这些agents.Methods：大鼠接受0.12 μ L/g体重利多卡因（0%，2%，10%，或20%）或布比卡因（0%，0.5%，2.5%，或5%）在蒸馏水通过鞘内导管的鞘内神经毒性。高渗透压的影响，也检查使用5%布比卡因在20%葡萄糖溶液（5%BG）和对照2 - 5%葡萄糖溶液。通过光镜和电镜检查L3脊髓、后根和前根以及马尾。结果：10%和20%利多卡因、5%布比卡因蒸馏水溶液（5%BDW）和5%BG处理组大鼠后根和后白色出现轴索变性，而2%利多卡因、0.5%和2.5%布比卡因、蒸馏水和25%葡萄糖溶液处理组大鼠后根和后白质均未出现轴索变性。20%利多卡因组的组织学损害较5%布比卡因组严重。后根损伤严重时，才出现后白色物质的破坏。5%BDW和5%BG的组织学结果无显著差异。结论：布比卡因和利多卡因引起的神经毒性损害在原发部位和延伸方式上难以区分，如起源于后根并延伸至后白色物质的轴突变性。利多卡因鞘内神经毒性大于布比卡因。
Background and Objectives: Clinical and laboratory studies suggest that lidocaine is more neurotoxic than bupivacaine. However, histological evidence of their comparative neurotoxicity is sparse. We thus pathologically and functionally compared the intrathecal neurotoxicity of these agents.Methods: Rats received 0.12 mu L/g body weight lidocaine (0%, 2%, 10%, or 20%) or bupivacaine (0%, 0.5%, 2.5%, or 5%) in distilled water via an intrathecal catheter. The influence of high osmolarity was also examined using 5% bupivacaine in 20% glucose solution (5% BG) and a control 2 5% glucose solution. The L3 spinal cord, the posterior and anterior roots, and the cauda equina were examined by light and electron microscopy. Walking behavior and sensory threshold were investigated as neurofunctional tests.Results: The posterior root and posterior white matter showed axonal degeneration in rats treated with 10% and 20% lidocaine and 5% bupivacaine in distilled water (5% BDW) and in 5% BG, but not in rats treated with 2% lidocaine, 0.5% and 2.5% bupivacaine, distilled water, or 25% glucose solution. The histological damages were more severe in 20% lidocaine-treated rats than in 5% bupivacaine-treated rats. The damage of posterior white matter was observed only when the posterior root was severely injured. No significant difference of histological findings was observed between 5% BDW and 5% BG. Functional abnormalities were found only in rats treated with 20% lidocaine.Conclusions: The neurotoxic lesions caused by bupivacaine and lidocaine were indistinguishable in the primary site and the extending pattern, such as axonal degeneration originating from the posterior roots and extending to the posterior white matter. The intrathecal neurotoxicity is greater in lidocaine than in bupivacaine.