Kalichman M W, Powell H C, Myers R R
Department of Anesthesiology, University of California San Diego, La Jolla 92093.
Acta Neuropathol. 1988;75(6):583-9. doi: 10.1007/BF00686203.
Nerve fiber injury and endoneurial edema were induced by the injection of the local anesthetic 2-chloroprocaine, tetracaine, procaine, etidocaine or mepivacaine into the soft tissue and fascia surrounding the sciatic nerve of Sprague-Dawley rats. Light microscopy demonstrated that the perineurial barrier was not mechanically damaged by the surgical procedure but, at 48 h post-injection, perineurial permeability was increased. Previous observations of leakage of horseradish peroxidase and the present report of neutrophils and eosinophils in the endoneurium indicate a disruption of blood-nerve barrier systems. Endoneurial edema was observed in the subperineurial, interstitial and perivascular regions. Axonal degeneration and demyelination occurred; the latter associated with accumulation of large lipid droplets in Schwann cells. Degranulation of mast cells, proliferation of fibroblasts and macrophage activity were noteworthy in affected areas. The findings are remarkable in that this is the first model of endoneurial edema by a neurotoxin which penetrates the perineurium, disrupting barrier system and inducing nerve fiber injury.
通过向Sprague-Dawley大鼠坐骨神经周围的软组织和筋膜注射局部麻醉剂2-氯普鲁卡因、丁卡因、普鲁卡因、依替卡因或甲哌卡因来诱导神经纤维损伤和神经内膜水肿。光学显微镜显示，神经束膜屏障未因手术操作而受到机械损伤，但在注射后48小时，神经束膜通透性增加。先前关于辣根过氧化物酶渗漏的观察以及本报告中神经内膜中嗜中性粒细胞和嗜酸性粒细胞的出现表明血神经屏障系统受到破坏。在神经束膜下、间质和血管周围区域观察到神经内膜水肿。轴突变性和脱髓鞘发生；后者与施万细胞中大量脂滴的积累有关。在受影响区域，肥大细胞脱颗粒、成纤维细胞增殖和巨噬细胞活性值得注意。这些发现很显著，因为这是第一个由神经毒素引起神经内膜水肿的模型，该神经毒素穿透神经束膜，破坏屏障系统并诱导神经纤维损伤。
