Different mechanisms of development and maintenance of experimental incision-induced hyperalgesia in human skin
Different mechanisms of development and maintenance of experimental incision-induced hyperalgesia in human skin
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DOI：
10.1097/00000542-200209000-00006
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发表时间：
2002-09-01
期刊：
影响因子：
8.8
通讯作者：
Namiki, A
中科院分区：
文献类型：
--
作者：
Kawamata, M;Watanabe, H;Namiki, A
背景：为了确定术后疼痛的机制，在一项涉及 17 名受试者的交叉、双盲、安慰剂对照人体研究中，评估了局部麻醉对手术切口引起的痛觉过敏的发生和维持的影响。方法：在每位受试者的前臂掌侧切开一个穿过皮肤、筋膜和肌肉的 4 毫米长的实验切口。在实验1中，在创伤前和创伤后将体积为0.2ml的1％利多卡因或盐水皮下注射到切口部位。在实验2中，在创伤前和创伤后在切口部位附近皮下注射0.2μl 1％利多卡因的5厘米长的皮肤条。切口制作后，对耀斑、自发性疼痛以及对点状机械刺激的原发性和继发性痛觉过敏进行评估。结果：创伤前注射利多卡因可防止自发性疼痛的发生以及在切开切口后立即（1 分钟）在切口部位周围发现的耀斑形成的发展。利多卡因比创伤后阻滞更有效地抑制原发性痛觉过敏，但仅限于切口后的前 4 小时。切前阻滞可防止继发性痛觉过敏的发生，而创伤后阻滞则不会显着影响完全发生的继发性痛觉过敏。耀斑形成的区域和继发性痛觉过敏的区域没有延伸到外伤前麻醉的皮肤带上，而外伤后阻滞并没有显着减少完全发展的继发性痛觉过敏的区域。结论：外伤前注射利多卡因比外伤后注射更有效地减少原发性痛觉过敏，但仅在切口后短时间内有效。继发性痛觉过敏的扩散是通过周围神经纤维介导的，但是当继发性痛觉过敏完全发展时，它变得不太依赖甚至独立于源自受伤部位的周围神经活动。
Background: To determine the mechanisms of postoperative pain, the effects of local anesthesia on development and maintenance of surgical incision-induced hyperalgesia were evaluated in a crossover, double-blinded, placebo-controlled human study using 17 subjects.Methods: An experimental 4-mm-long incision through skin, fascia, and muscle was made in the volar forearm of each subject. In experiment 1, 1% lidocaine or saline in a volume of 0.2 nil was subcutaneously injected into the incision site pretraumatically and posttraumatically. In experiment 2, a 5-cm-long strip of skin was subcutaneously injected with 0.2 nil of 1% lidocaine near the incision site pretraumatically and posttraumatically. Flare, spontaneous pain, and primary and secondary hyperalgesia to punctate mechanical stimuli were assessed after the incision had been made.Results: Pretraumatic lidocaine injection prevented the occurrence of spontaneous pain and development of flare formation that was found surrounding the incision site immediately (1 min) after the incision had been made. The lidocaine suppressed primary hyperalgesia more effectively than did posttraumatic block, but only for the first 4 h after the incision. The preincision block prevented development of secondary hyperalgesia, whereas posttraumatic block did not significantly affect the fully developed secondary hyperalgesia. The area of flare formation and the area of secondary hyperalgesia did not extend over the strip of the skin that had been pretraumatically anesthetized, whereas the posttraumatic block did not significantly reduce the area of fully developed secondary hyperalgesia.Conclusions: Pretraumatic injection of lidocaine reduces primary hyperalgesia more effectively than does posttraumatic injection, but only for a short period after incision. The spread of secondary hyperalgesia is mediated via peripheral nerve fibers, but when secondary hyperalgesia has fully developed, it becomes less dependent on or even independent of peripheral neural activity originating from the injured site.