Physiologic Mechanisms by Which Local Anesthetics May Cause Injury to Nerve and Spinal Cord
Physiologic Mechanisms by Which Local Anesthetics May Cause Injury to Nerve and Spinal Cord
复制标题
局部麻醉药可能导致神经和脊髓损伤的生理机制
DOI：
10.1136/rapm-00115550-199318061-00012
复制
发表时间：
1993
影响因子：
5.1
通讯作者：
M. Kalichman
中科院分区：
文献类型：
--
作者：
M. Kalichman
Objective.回顾局麻药引起神经损伤的可能生理机制的证据。方法.已发表的临床病例报告，在动物体内和体外实验研究，进行了审查。纳入了与局部麻醉神经毒性的可能机制直接相关的报告。结果有基础和临床证据表明，局部麻醉药可引起神经损伤。神经损伤可能由轴突或许旺细胞的直接毒性引起，或者可能继发于神经微环境的破坏。虽然这些可能性都得到了已发表的实验的支持，但轴突损伤是持续性神经功能缺损的最可能解释，例如那些被认为是由局部麻醉剂的临床使用引起的。无论是直接还是间接的伤害，以及它发生的确切机制，都只得到了有限的研究。结论.在极少数情况下，局部麻醉剂的临床使用与神经系统疾病有关。有最好证据的毒性生理机制是抑制快速轴突运输、破坏轴突细胞骨架、轴突变性和缺血性神经损伤。局麻药对神经血流量的影响可能与抑制内皮依赖性血管舒张或中断血管舒张素的合成有关。预防和治疗由局部麻醉剂引起的神经损伤需要关于局部麻醉剂直接神经毒性的生理和分子机制的信息。
Objective. Review evidence for possible physiologic mechanisms by which local anesthetics cause nerve injury was reviewed. Methods. Published clinical case reports, and both in vivo and in vitro experimental studies in animals, were reviewed. Reports with direct bearing on possible mechanisms of local anesthetic neurotoxicity were included. Results. There is basic and clinical evidence that local anesthetics can cause nerve injury. Nerve injury may result from direct toxicity to the axon or Schwann cell, or may be secondary to disruption of the nerve microenvironment. Although each of these possibilities is supported by published experiments, injury to the axon is the most likely explanation for persistent neurologic deficits, such as those believed to result from clinical use of local anesthetics. Whether the injury is direct or indirect, and the precise mechanism by which it occurs, has received only limited study. Conclusions. In rare instances, the clinical use of local anesthetics is associated with neurologic morbidity. The physiologic mechanisms of toxicity for which there is the best evidence are inhibition of fast axonal transport, disruption of the axonal cytoskeleton, axonal degeneration, and ischemic nerve injury. The effects of local anesthetics on nerve blood flow may be related to inhibition of endothelium-dependent vasodilation or interruption of the synthesis of vasodilating prostaglandins. Both the prevention and the treatment of nerve injury caused by local anesthetics requires information that is not yet available about the physiologic and molecular mechanisms for direct neural toxicity of local anesthetics.