Yamamoto T, Shimoyama N, Asano H, Mizuguchi T
Department of Anesthesiology, School of Medicine, Chiba University, Japan.
Anesth Analg. 1995 Mar;80(3):515-20. doi: 10.1097/00000539-199503000-00014.
Nerve ischemia induces wallerian degeneration and peripheral neuropathy, the nerve constriction injury induces thermal hyperesthesia. Nerve ischemia is one possible mechanism in the development of thermal hyperesthesia in the nerve constriction injury model. Prostaglandin E1 increases tissue blood flow. In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E1 derivative. A nerve constriction injury model was created by making four loose ligations around the rat sciatic nerve, which induces thermal hyperesthesia in the ligated paw in 2-5 days. OP-1206, was administered six times (Day 7, one time; Day 8, two times; Day 9, two times; Day 10, one time). A single administration of OP-1206 had no effect on the thermal hyperesthesia. Six hours after the sixth-administration of OP-1206, the level of the thermal hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration. These data indicate that nerve ischemia plays an important role in maintaining the thermal hyperesthesia induced by nerve constriction injury in the rat.
神经缺血会导致沃勒变性和周围神经病变，神经挤压伤会诱发热感觉过敏。神经缺血是神经挤压伤模型中热感觉过敏发生发展的一种可能机制。前列腺素E1可增加组织血流量。在本研究中，作者通过口服前列腺素E1衍生物OP-1206，研究神经缺血在维持神经挤压伤所致热感觉过敏中的作用。通过在大鼠坐骨神经周围进行四次宽松结扎建立神经挤压伤模型，该模型在2至5天内可诱发结扎爪的热感觉过敏。OP-1206给药六次（第7天，1次；第8天，2次；第9天，2次；第10天，1次）。单次给予OP-1206对热感觉过敏无影响。在第六次给予OP-1206后6小时，热感觉过敏水平呈剂量依赖性减弱，且该效应在最后一次给药后持续超过1天。这些数据表明，神经缺血在维持大鼠神经挤压伤所致热感觉过敏中起重要作用。
