Luukko M, Konttinen Y, Kemppinen P, Pertovaara A
Department of Physiology, University of Helsinki, Finland.
Exp Neurol. 1994 Jul;128(1):143-54. doi: 10.1006/exnr.1994.1122.
In the current investigation we examined a peripheral mononeuropathy induced by four loose ligatures around the sciatic nerve. The nerve was treated with lidocaine or saline before implementing the ligatures (silk or chromic gut). The latency of the hindlimb withdrawal to noxious mechanical and radiant heat stimuli was tested under light pentobarbital anesthesia 3-10 days following the surgery. A latency/threshold difference > or = 15% between the hindlimbs was considered to represent a change in the nocifensive response. The adapting skin temperature of the hindlimbs was also measured. Pieces of hindpaw skin and the sciatic nerve were taken for histological evaluation. The results indicate that the incidence of hyperalgesia induced by a constriction mononeuropathy depended on the noxious submodality tested, and that the thermal and mechanical hyperalgesia were not coupled in all cases. Use of only one test modality led to false negative results. Furthermore, mononeuropathy-induced changes in the adapting skin temperature produced a considerable number of false positive results (an artefactual hyperalgesia) when radiant heat alone was used to determine the nocifensive withdrawal latency without paying attention to the abnormality of the skin temperature. A preemptive lidocaine treatment of the sciatic nerve before the nerve ligation significantly reduced the incidence of mononeuropathy-induced hyperalgesia. The nerve ligation material (silk vs chromic gut) was not a significant factor for the development of hyperalgesia induced by a constriction injury of a peripheral nerve. In histological evaluation the constriction injury-induced damage of the sciatic nerve was verified, and the inflammatory reaction caused by chromic gut was not stronger than that caused by silk ligatures. In general, immunohistochemical staining for substance P decreased whereas that for VIP increased. The results support the hypothesis that ligation-induced mechanical trauma and the afferent barrage induced by it, especially during the perioperative period, plays an important role in the development of postoperative hyperalgesia.
在当前的研究中，我们检查了由坐骨神经周围四条松结扎线诱导的周围性单神经病。在实施结扎（丝线或铬制肠线）之前，用利多卡因或生理盐水处理神经。在手术后3 - 10天，在轻度戊巴比妥麻醉下测试后肢对有害机械和辐射热刺激的退缩潜伏期。后肢之间的潜伏期/阈值差异≥15%被认为代表伤害性反应的变化。还测量了后肢适应性皮肤温度。取后爪皮肤和坐骨神经组织块进行组织学评估。结果表明，压迫性单神经病诱导的痛觉过敏发生率取决于所测试的有害亚模式，并且热痛觉过敏和机械痛觉过敏在所有情况下并非都相关联。仅使用一种测试模式会导致假阴性结果。此外，当仅使用辐射热来确定伤害性退缩潜伏期而不关注皮肤温度异常时，单神经病诱导的适应性皮肤温度变化会产生大量假阳性结果（人为痛觉过敏）。在神经结扎前对坐骨神经进行预防性利多卡因治疗可显著降低单神经病诱导的痛觉过敏发生率。神经结扎材料（丝线与铬制肠线）对于周围神经压迫性损伤诱导的痛觉过敏发展不是一个重要因素。在组织学评估中，证实了压迫性损伤对坐骨神经的损害，并且铬制肠线引起的炎症反应并不比丝线结扎引起的更强。一般来说，P物质的免疫组化染色减少而血管活性肠肽的染色增加。这些结果支持这样的假设，即结扎诱导的机械创伤及其诱导的传入冲动，特别是在围手术期，在术后痛觉过敏的发展中起重要作用。
