牵张性脊髓损伤机理的实验研究

Experimental study on the pathogenesis of traction injury of the spinal cord

探讨牵张性脊髓损伤的病理机制。方法用脊髓组织内丙二醛（ＭＤＡ）和过氧化物歧化酶（ＳＯＤ）定量分析等技术，附以组织形态学观察，评定动物模型的脊髓功能，进而研究牵张性脊髓损伤的机理。结果随着牵开负荷的增大和作用时间的延长，脊髓微血管充盈缺损、痉挛直至破裂出血，脊髓内ＳＯＤ下降，ＭＤＡ含量升高。５０％５分钟组及５０％１０分钟组脊髓功能下降，与对照组相比有显著性差异。结论由脊髓血管改变所致的缺血是牵张性脊髓损伤的主要原发机制。

bjective To explore the pathogenesis of the traction injury of spinal cord.Methods Forty rabbits were randomly divided into four groups,according to the amplitude decreasing of SCEP wave.The function of the spinal cord,the amount of Malonylodialdehyde(MDA)and SuperoxideDistumase(SOD) of the spinal cord tissue and the pathomorphological changes of the spinal cord were observed.Results SOD in the the spinal cord was decreased and MDA content elevated.Significant difference in the function of the spinal cord was shown in 50% 5min group and 50% 10min group,as compared with the control.Conclusion:The spinal cord ischemia caused by the change of the vessels in the spinal cord was the main pathogenesis of the traction injury of the spinal cord and the lipid peroxidation mediated by freeradical production would make the traction injury of the spinal cord worse from its secondary pathological changes.