Pathphysiologic mechanism of radicular pain in lumbar disc herniation.

本研究的目的是确定腰椎间盘突出症中神经根性疼痛的病理生理机制。在本实验模型中，自体髓核（NP）和纤维环（AF）移植到腰神经根后，大鼠产生机械和热痛觉过敏，这是一种与疼痛相关的行为。,分别。硬膜外注射选择性磷脂酶A_2 （PLA_2）抑制剂可使对有害机械刺激的超敏反应消失。通过硬膜外注射生理盐水和一氧化氮（NO）合成酶抑制剂来减轻和消除AF引起的热痛觉过敏。应用逆转录聚合酶链反应技术，测定大鼠神经根和背根神经节中白细胞介素-1 β (il -1 β)、白细胞介素-6（IL-6）、PLA_2和诱导型NO合成酶（iNOS）基因的表达。仅NP处理大鼠il -1 β、PLA_2和iNOS信使rna的表达在术后1周明显升高，在术后2周和4周降至基础水平。术后4周检测NP组IL-6的表达。本研究还旨在阐明机械压迫神经根和NP产生疼痛的机制。NP组和蚕丝结扎产生机械压迫的蚕丝+NP组大鼠分别出现机械痛敏和热痛敏。组织学分析显示，与NP组相比，丝和丝+NP组神经根上的大直径髓鞘轴突较少，小直径髓鞘轴突较多。提示椎间盘诱导的il、PLA_2、NO等化学介质参与了腰椎间盘突出症疼痛性神经根病的病理生理机制，而非神经根的组织学改变。

The purpose of this study was to determine pathophysiological mechanism of radicular pain in lumbar disc herniation. In this experimental model, autologous nucleus pulposus (NP) and anulus fibrosus (AF) transplanted to lumbar nerve roots produced mechanical and thermal hyperalgesia, which is a pain related behavior in the rat., respectively. Epidural injection of a selective inhibitor for phospholipase A_2 (PLA_2) resulted in the disappearance of hypersensitivity to noxious mechanical stimuli. Thermal hyperalgesia produced by application of the AF was abated and abolished by epidural injections of saline and one of the inhibitors for nitric oxide (NO) synthase, respectively. Utilizing a reverse transcription polymerase chain treaction echnique, the expression of interleukin-1beta (IL-1beta), interleukin-6(IL-6), PLA_2 and inducible NO synthase (iNOS) genes was evaluated in the nerve root and dorsal root ganglion. The expression of IL-1beta, PLA_2 and iNOS messenger RNAs only in rats treated with the NP were clearly increased at 1 week postoperatively and decreased to the basal level at 2 and 4 weeks postoperatively. However, the expression of IL-6 in the NP group were detected by 4 weeks postoperatively. This study was also designed to elucidate the pain mechanism produced by mechanical compression of the nerve root and NP.Rats in the NP group and the silk+NP group, which mechanical compression was produced by silk ligation, showed evidence of mechanical and thermal hyperalgesia, respectively. Histological analysis revealed that there were less of the larger and more of the smaller diameter myelinated axons on the nerve roots in both of the silk and silk+NP groups, compared with that in the NP groups. These results suggest that chemical mediators such as ILs, PLA_2 and NO,induced by intervertebral discs, are involved in the pathophysiological mechanisms of painful radiculopathy in lumbar disc herniations but not histological changes of the nerve root.