大鼠低氧血症性二次脑损伤模型的建立

A rat model of secondary hypoxic insult after traumatic axonal injury

目的 建立创伤性轴索损伤（TAI）合并低氧血症性二次脑损伤（SBI）大鼠模型,探讨低氧血症SBI损伤机制.方法 应用自制的TAI致伤装置,对致伤后大鼠给予10％浓度氧30 min制成低氧血症性SBI模型,对大鼠伤后生理学、病理学进行分析评价,同时测定伤后脑组织的丙二醛（MDA）和超氧化物岐化酶（SOD）水平.结果 合并低氧血症SBI大鼠伤后海马存活神经元减少（104个比134、186个）,脂质过氧化（LPO）增强（24 h时MDA：7.60 nmol/mg蛋白比5.43、2.77 nmol/mg蛋白;SOD：77.20 U/mg蛋白比99.93、116.37 U/mg蛋白）,与单纯TAI组及低氧血症组比较差异均有统计学意义（P＜0.05）.结论 该模型较好的复制了低氧血症SBI的临床特征,具有良好的稳定性和重复性.

Objective To establish a secondary brain injury （SBI） animal model,with hypoxic insult following traumatic axonal injury （TAI）,and to explore the underlying mechanism how post-traumatic hypoxia exacerbates primary brain injury.Methods Homemade TAI device was applied.After injury the rats were given 10% oxygen concentration for 30 min,and the hypoxemia SBI model was established.The physiologic and pathologic changes were analyzed and evaluated,and the brain tissue malondialdehyde （MDA） and superoxide dismutase （SOD） levels were determined in post-traumatic rats.Results Compared to TAI-only and hypoxia-only groups,TAI plus hypoxia significantly decreased the number of survived hippocampal neurons （104 vs.134,186）,and as well as enhanced lipid peroxidation （LPO） （at 24 h,for M DA content：7.60 vs.5.43,2.77 nmol/mg prot; for SOD activity：77.20 vs.99.93,116.37 U/mg prot）.Conclusion This model replicated the clinical features of the SBI with hypoxemia,and has a good stability and repeatability.