【摘要】：目的:為了研究交感神經(jīng)系統(tǒng)對(duì)神經(jīng)病理性疼痛的調(diào)控機(jī)理。我們?cè)诖笫蟮穆詨浩缺掣窠?jīng)節(jié)(chronic compression of dorsal root ganglion,CCD)模型上給予交感神經(jīng)阻斷劑胍乙啶(Guanethidine,GU)后,觀察實(shí)驗(yàn)大鼠背根神經(jīng)節(jié)(dorsal root ganglion,DRG)內(nèi)交感神經(jīng)芽生的分布狀況,以及后者對(duì)實(shí)驗(yàn)大鼠疼痛行為學(xué)的影響,并探討交感神經(jīng)芽生對(duì)神經(jīng)病理性疼痛的作用及其機(jī)制。方法:1、將雄性SD大鼠隨機(jī)分為Sham組和CCD組,采用von Frey纖維絲監(jiān)測(cè)其50%機(jī)械性刺激縮足反射閾值的改變;并且于造模后第28天取各組實(shí)驗(yàn)大鼠背根神經(jīng)節(jié),甲醛固定后,做冰凍切片,采用免疫熒光染色技術(shù)研究大鼠背根神經(jīng)節(jié)內(nèi)交感神經(jīng)芽生的分布變化趨勢(shì),分析其與疼痛行為之間的關(guān)系。2、將雄性SD大鼠隨機(jī)分為Sham組、CCD+NS組、CCD+Guanethidine組,采用von Frey纖維絲觀察各組大鼠的50%機(jī)械性刺激縮足反射閾值的改變,研究術(shù)前經(jīng)腹腔途徑注射交感神經(jīng)阻斷劑胍乙啶對(duì)慢性壓迫背根神經(jīng)節(jié)模型大鼠機(jī)械性刺激痛覺過敏行為的影響,并且于造模后第28天取各組實(shí)驗(yàn)大鼠背根神經(jīng)節(jié),經(jīng)過甲醛固定后,做冰凍切片,再應(yīng)用免疫熒光染色技術(shù)研究試驗(yàn)大鼠背根神經(jīng)節(jié)內(nèi)交感神經(jīng)芽生分布的變化趨勢(shì),分析其與實(shí)驗(yàn)大鼠機(jī)械性刺激疼痛行為之間的關(guān)系,探討胍乙啶對(duì)疼痛和炎性反應(yīng)的影響。結(jié)果:1、建立慢性壓迫背根神經(jīng)節(jié)模型后,實(shí)驗(yàn)大鼠雙側(cè)后肢50%機(jī)械性刺激縮足反射閾值與Sham組實(shí)驗(yàn)大鼠相比較明顯下降(P0.01)。在交感神經(jīng)芽生分布這一方面,慢性壓迫背根神經(jīng)節(jié)造模術(shù)后第28天交感神經(jīng)芽生的分布明顯增多(P0.01),且明顯高于Sham組,具有統(tǒng)計(jì)學(xué)意義。2、經(jīng)腹腔注射交感神經(jīng)阻斷劑胍乙啶可明顯提高背根神經(jīng)節(jié)慢性壓迫模型大鼠的機(jī)械性刺激縮足閾值,與CCD+NS組相比,具有明顯差異;而經(jīng)腹腔注射生理鹽水對(duì)正常大鼠的50%機(jī)械性刺激縮足反射閾值并無明顯影響。免疫熒光染色實(shí)驗(yàn)結(jié)果顯示,胍乙啶可使慢性壓迫背根神經(jīng)節(jié)模型大鼠背根神經(jīng)節(jié)上的交感神經(jīng)芽生分布明顯減少,與CCD+NS組實(shí)驗(yàn)大鼠相比,具有明顯的統(tǒng)計(jì)學(xué)差異。結(jié)論:1、交感神經(jīng)芽生在受慢性壓迫的背根神經(jīng)節(jié)上的分布明顯增多,而且慢性持續(xù)性壓迫背根神經(jīng)節(jié)能顯著降低大鼠的機(jī)械性刺激痛閾,提示背根神經(jīng)節(jié)內(nèi)的交感神經(jīng)芽生可能參與了大鼠神經(jīng)病理性疼痛的形成和維持。2、交感神經(jīng)阻斷劑胍乙啶可明顯抑制由慢性壓迫背根神經(jīng)節(jié)模型引起的大鼠神經(jīng)病理性疼痛,同時(shí)也減少了受慢性壓迫的背根神經(jīng)節(jié)上交感神經(jīng)芽生的分布,進(jìn)一步說明大鼠背根神經(jīng)節(jié)內(nèi)出現(xiàn)的交感神經(jīng)芽生與神經(jīng)病理性疼痛形成和維持可能存在關(guān)聯(lián)。
[Abstract]:Objective: to study the regulation mechanism of sympathetic nervous system on neuropathic pain. We treated the rat model of chronic compression of dorsal root ganglion (chronic compression of dorsal root ganglion,CCD) with aganidine (Guanethidine,GU), a sympathetic nerve blocker, and observed (dorsal root ganglion, in the experimental rat dorsal root ganglion (DRG). The distribution of sympathetic nerve buds in DRG and the effect of the latter on the pain behavior of experimental rats were also discussed. The effects of sympathetic nerve buds on neuropathic pain and its mechanism were also discussed. Methods: 1. Male SD rats were randomly divided into Sham group and CCD group. The changes of reflex threshold of 50% mechanical stimulation were monitored by von Frey filament. On the 28th day after the model, the experimental rats' dorsal root ganglia were taken and fixed with formaldehyde, then frozen sections were made. The distribution of sympathetic nerve buds in the dorsal root ganglion of rats was studied by immunofluorescence staining. 2the male SD rats were randomly divided into Sham group (, CCD NS group) and, CCD Guanethidine group (, CCD NS group). The changes of reflex threshold of 50% mechanical stimulation in each group were observed with von Frey filament. To study the effect of intraperitoneal injection of guanidine, a sympathetic nerve blocker, on hyperalgesia in rats with chronic compression of dorsal root ganglion (DRG). After formalin fixation, frozen sections were made, and then the distribution of sympathetic nerve buds in dorsal root ganglion of experimental rats was studied by immunofluorescence staining, and the relationship between the distribution of sympathetic nerve buds and the pain behavior of mechanical stimulation in experimental rats was analyzed. To investigate the effect of guanidine on pain and inflammatory response. Results: 1. After establishing the model of chronic compression of dorsal root ganglion, the reflex threshold of 50% mechanical stimulation on both hind limbs of experimental rats was significantly lower than that of experimental rats in Sham group (P0.01). In the distribution of sympathetic nerve buds, the distribution of sympathetic nerve buds increased significantly on the 28th day after chronic compression of dorsal root ganglion model (P0.01), and was significantly higher than that in Sham group, which was statistically significant. Intravenous injection of guanidine, a sympathetic nerve blocker, significantly increased the threshold of mechanical stimulation in rats with chronic compression of dorsal root ganglion (DRG), which was significantly different from that in CCD NS group. However, intraperitoneal injection of normal saline had no significant effect on the reflex threshold of 50% mechanical stimulation in normal rats. The results of immunofluorescence staining showed that guanidine could significantly reduce the distribution of sympathetic nerve buds in the dorsal root ganglion of rats with chronic compression of dorsal root ganglion (DRG), which was significantly different from that of the experimental rats in CCD NS group. Conclusion: 1. The distribution of sympathetic nerve buds on the dorsal root ganglion (DRG) under chronic compression was significantly increased, and the energy saving of chronic continuous compression of DRN significantly decreased the pain threshold of mechanical stimulation in rats. These results suggest that sympathetic nerve sprouting in dorsal root ganglion may be involved in the formation and maintenance of neuropathic pain in rats. The sympathetic blocker guanidine inhibited the neuropathic pain induced by chronic compression of the dorsal root ganglion in rats, and also reduced the distribution of sympathetic nerve buds on the dorsal root ganglion under chronic compression. It is further suggested that the sympathetic ganglia in the dorsal root ganglion of rats may be associated with the formation and maintenance of neuropathic pain.
【學(xué)位授予單位】：廣東藥科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R402

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