兔牵张性脊髓损伤的病理形态学改变

为了探索牵张性脊髓损伤的病理机制。我们选用４０只健康日本大耳白兔，随机分成对照组、体感皮层诱发电位波幅下降３０％组，５０％５分钟组、５０％１０分钟组。通过对动物运动功能评价、脊髓组织内丙二醛（ｍａｌｏｎｙｌｏｄｉａｌｄｅｈｙｄｅ，ＭＤＡ）和过氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅｄｉｓｔｕｍａｓｅ，ＳＯＤ）定量分析、组织形态等方法，研究牵张性脊髓损伤。结果显示：随着撑开负荷增加和作用时间延长。导致脊髓灰白质内血管充盈不足、痉挛直至血管破裂出血。脊髓组织内ＳＯＤ含量下降、ＭＤＡ含量升高。５０％５分钟组和５０％１０分钟组的Ｔａｒｌｏｖ评分障碍率和Ｍｏｌｔ斜板障碍率增大。与对照组相比，其差异有显著性。研究证明脊髓血管的改变是牵张性脊髓损伤的早期病理机制，而自由基介导的脂质过氧化反应则参与了牵张性脊髓损伤的继发性损害过程。

Pathomorphological Changes of Traction Injury of Spinal Cord in Rabbit

In order to explore the pathomorphological changes of traction injury to the spinal cord, 40 rabbits were randomly divided into four groups according to the amount of the decreasing of the amplitude of SCEP P1 wave. The function of spinal cord was assessed, the amount of MDA and SOD of spinal cord tissue was determined and pathomorphological changes of spinal cord were observed. The results showed that the spinal cord ischemia which was caused by the spasm and bleeding in the vessels of spinal cord was the main pathomorphological changes of traction injury to the spinal cord, the lipid peroxidation mediated by free radical production would make the traction injury of the spinal cord worse from secodary pathological damage.