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背根的慢性炎症和压迫导致大鼠椎间盘突出引起的坐骨神经痛。

Chronic inflammation and compression of the dorsal root contribute to sciatica induced by the intervertebral disc herniation in rats.

作者信息

Hou Shu-Xun, Tang Jia-Guang, Chen Hui-Sheng, Chen Jun

机构信息

Institute of Orthopedics, 304 Hospital of PLA, 51 Fucheng Road, Beijing 100037, PR China.

出版信息

Pain. 2003 Sep;105(1-2):255-64. doi: 10.1016/s0304-3959(03)00222-7.

Abstract

The pathophysiological mechanisms underlying sciatica and back pain are not well understood. In the present study, a sciatica model was developed to investigate the contributions of inflammation and compression of the dorsal root (DR). The procedure used autologous disc to apply direct pressure to the L5 DR (disc compression, DC group). For control, five additional groups were included: (1). mechanical compression of L5 DR without disc (compression, CP group); (2). epidurally placed disc without mechanical compression (disc group); (3). epidurally placed nucleus pulposus (NP) without mechanical compression (NP group); (4). epidurally placed annulus fibrosus (AF) without mechanical compression (AF group) and (5). sham group. The paw withdrawal latency to heat stimulation, paw withdrawal threshold to mechanical stimulation, body weight, and motor function were determined pre- and post-surgery. It was observed that all experimental groups with the exception of the sham group showed a progressive and prolonged mechanical hyperalgesia with the DC group having the strongest effect. Furthermore, the disc group showed a greater mechanical hyperalgesia with earlier onset in comparison with the CP group and disc, AF, and NP groups developed thermal hyperalgesia in addition to mechanical hyperalgesia following surgery. Finally, rats in all groups showed normal motor function and body weight increase. These data suggest that this model is suitable to investigate the mechanisms of sciatica and inflammation as well as mechanical compression is involved in the pathogenesis of this condition. Moreover, AF and NP may contribute similarly to the development of sciatica and back pain.

摘要

坐骨神经痛和背痛的病理生理机制尚未完全明确。在本研究中,我们建立了一个坐骨神经痛模型,以探究背根神经节(DR)炎症和受压的作用。该实验通过自体椎间盘直接压迫L5背根神经节(椎间盘压迫组,DC组)。作为对照,另外设置了五组:(1)不使用椎间盘对L5背根神经节进行机械压迫(压迫组,CP组);(2)硬膜外放置椎间盘但不进行机械压迫(椎间盘组);(3)硬膜外放置髓核(NP)但不进行机械压迫(NP组);(4)硬膜外放置纤维环(AF)但不进行机械压迫(AF组);(5)假手术组。在手术前后分别测定热刺激缩爪潜伏期、机械刺激缩爪阈值、体重和运动功能。结果发现,除假手术组外,所有实验组均出现进行性且持续时间较长的机械性痛觉过敏,其中DC组效应最强。此外,与CP组相比,椎间盘组机械性痛觉过敏更明显且出现时间更早,AF组和NP组在术后除机械性痛觉过敏外还出现了热痛觉过敏。最后,所有组大鼠的运动功能均正常,体重也均增加。这些数据表明,该模型适用于研究坐骨神经痛机制,炎症以及机械压迫参与了该病的发病过程。此外,AF和NP在坐骨神经痛和背痛的发生中可能发挥相似作用。

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