【作者】 张增祥；

【导师】 张克亮； 张哲敏； 周君琳；

【作者基本信息】 河北医科大学 ， 外科学， 2002， 硕士

【摘要】 目的：通过复制坐骨神经卡压模型，探讨周围神经卡压对脊髓神经元数目及超微结构的影响，观察神经胶质细胞的变化。 方法：选用成年健康SD大鼠50只，雌雄不限，体重200～250g，采用经典的大鼠坐骨神经慢性卡压模型，1％戊巴比妥钠0.3ml／100g腹腔注射麻醉，左侧为实验组，右侧为对照组，在实验侧显露大腿后侧坐股神经，长10mm、内径1.2mm的硅胶管纵行剖开包裹神经，9-0的无损伤缝线缝合管壁3针，对照组不作处理，随着大鼠的生长，坐骨神经逐渐被卡压。模型制作完毕后，按不同时间段随机分成5组，每组10只，分笼喂养，分别于术后12周、18周、24周、30周、36周再次腹腔注射麻醉，开胸，降主动脉插管，下腔静脉胸段剪开放血，肝素盐水(1250u／100ml)灌注至流出液体为无色时改用10％甲醛液150ml滴注，灌注时间40分钟。后入路取材(L4—L6脊髓)。分别固定，切片，在光镜和透射电镜下观察神经元的超微结构，神经元计数，计算实验侧与对照侧神经元数目之比(L／R)，同时观察神经胶质细胞的变化。 结果：术后12周，脊髓前角神经元数目无明显变化，术后18周、24周、30周、36周神经数目分别减少7.46％、12.24％、16.83％、20.98％。术后18周HE染色组发现 中文摘要 ‘卫星现象’。30周时位于lamina IX区的前角细胞明显减少。局部可见大量神经胶质细胞。饿酸染色组24周出现脱髓鞘现象，且脱髓鞘发生在灰质区。呈逐渐加重趋势。12周时电镜观察可见脊髓前角细胞内线粒体肿胀，内质网扩张，核仁清晰，染色质分布均匀，呈常染色质状态。18周时线粒体肿胀加剧，内质网进一步扩张，溶酶体消夫，染色质边集，异染色质增多，24周、30周、36周细胞逐渐减少，核变小，深染浓缩，细胞空化，核周膜模糊不清，神经细胞趋向坏死。术后30周，神经胶质细胞内细胞器明显减少，细胞膜结构不清，异染色质边集。 结论：实验结果表明：坐骨神经卡压后，相应节段脊髓前角a运动神经元超微结构发生改变，神经元数目减少，并随卡压时间的延长，卡压程度的加重而加重，因此认为时于周围神经卡压应尽早的解除卡压，以减少或消除神经元结构改变和死亡，提高疗效。与此同时应充分认识神经胶质细胞在神经损伤旱期的修复作用一经胶质细胞的修复作用在什么条件下转变成抑制性屏障作用及如何延长修复作用时间有待进一步探讨。更多还原

【Abstract】 Objective: To investigate the effect of peripheral nerve compression on the ultrastructural changes and the number of neurons and observe the changes of glial cell in rats.Methods: A chronic nerve compression animal model was made according the method described by Machinnonic, the animals were anesthetized using an abdominal injection of sodium thiopental (0.3ml/100g). The procedures were conducted using a surgical microscope under 10 magnifications and by the same person. The left sciatic nerve was exposed and identified, a 10mm length of silastic tub with an internal diameter of 1.2mm was cut longitudinally and placed around the nerve. The cut of tub was sewn closed with 9-0 sutures and the tub was reconstituted to its original diameter. The procedures were conducted on the left side, the right side served as a within -subject control. The rats were randomly sacrificed in 12,18,24,30 and 36 weeks after operation .The animals were anesthetized again at different interval after sciatic nerve compression and spinals (L4-6) were cut from thebackhand and stained respectively. The ultrastructural changes and the number of neuron and glial cell of the corresponding spinal segments were observed under light microscope and transmission electron microscope, The number of neurons were counted to calculate the percentage by comparing the experimental side with the control side,Results: light microscope: After sciatic nerve compression of 12 weeks, the number of neurons were no obviously decrease while after sciatic nerve compression of 18,24,30 and 36 weeks ,the number of neurons were decreased 7.46 %> 12.24 %, 16.83 %> 20.98 % respectively. Satellitosis was observed after sciatic nerve compression of 18 weeks in the sections stained with hematoxylin-eosion. The number of neurons locating lamina Ix is decreased significant comparing the group of control side. Trasmission electron microscope: After sciatic nerve compression of 12 weeks the swelled mitochondrion and dilatation endoplasmic was seen, the nucleolus is clear, the chromatin is distributed proportionate. After sciatic nerve compression of 18 weeks, the mitochondrion became more and more swell and the endoplasmic enlarged further more the lysosme has vanished, chromatin margination was seen and heterochromation formed. After sciatic nerve compression of 24,30 and 36 weeks The mitochordrion and endoplasmic decreased gradually, the nucleus becamesmaller, dark stained and some of them were condensed. The nerve cell became cavitation, the perinuclear membrane became indistinct and even the death might occur.Conclusions: The experimental results showed as following: After the sciatic nerve were compressed, the number of neuron and ultrastructure of neurons might undergo changes and even the death might occur. These changes might be aggravated as the time of compression was prolonged and the compression force was increased. It was conclude that for nerve compression decompression should be done as early as possible in order to avoid or minimize the ultrastructural changes of the neuron. In the meantime we should recognize the repair function of glial cell in early stage of nerve lesion. What is the condition that the repair function of glial cells transform inhibition barrier and how to prolong the stage of its repair function, which need make further study.更多还原