| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
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.
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