Takenami T, Yagishita S, Asato F, Hoka S
Department of Anesthesiology, Kitasato University, Kanagawa, Japan.
Reg Anesth Pain Med. 2000 Jul-Aug;25(4):372-9. doi: 10.1053/rapm.2000.6444.
Neurotoxicity of intrathecally administered local anesthetics is generating increased interest. This study was designed to examine the histopathologic effects of intrathecally administered tetracaine.
Sixty Wistar rats randomly received either 20%, 10%, 5%, 3%, 1%, 0.5%, or 0% tetracaine dissolved in 10% glucose solution or no solution via a chronically implanted intrathecal catheter. The spinal cord at L1, posterior and anterior roots and cauda equina were excised 5 days later, sectioned, processed, and prepared for light and electron microscopic examinations.
Rats treated with tetracaine at 10% or 20% developed lesions in the posterior white matter and posterior roots. Rats injected with 3% or 5% tetracaine developed lesions, which began in the posterior roots close to the spinal cord and extended to the posterior white matter. The lesions were characterized by axonal degeneration. Injections of < or =1% of tetracaine did not cause any pathological changes.
Our results suggest that the initial target of intrathecal tetracaine neurotoxicity may be the posterior roots at their entry into the spinal cord, where the axons are devoid of myelin sheath and thus representing a sensitive area for neurotoxic change.
鞘内注射局部麻醉药的神经毒性越来越受到关注。本研究旨在探讨鞘内注射丁卡因的组织病理学效应。
60只Wistar大鼠通过长期植入的鞘内导管随机接受溶解于10%葡萄糖溶液中的20%、10%、5%、3%、1%、0.5%丁卡因或无溶液注射。5天后切除L1节段的脊髓、后根和前根以及马尾，进行切片、处理，准备用于光镜和电镜检查。
接受10%或20%丁卡因治疗的大鼠后白质和后根出现病变。注射3%或5%丁卡因的大鼠出现病变，始于靠近脊髓的后根，并延伸至后白质。病变的特征为轴突退变。注射≤1%丁卡因未引起任何病理变化。
我们的结果表明，鞘内丁卡因神经毒性的初始靶点可能是后根进入脊髓的部位，此处的轴突没有髓鞘，因此是神经毒性变化的敏感区域。
