大鼠缺血性二次脑损伤模型的建立

Experimental study on animal model of diffuse brain injury with ischemic secondary brain insult in rats

目的 建立弥漫性脑损伤 (diffusebraininjury ,DBI)合并二次脑损伤 (secondarybraininsult,SBI)大鼠模型 .方法 在Marmarou模型基础上 ,双侧颈总动脉结扎 30min,制成缺血性SBI模型 ,测定大鼠脑组织含水量及观察室上区皮层损伤神经元数变化 .结果 DBI合并SBI组大鼠死亡率 (5 4 8% )约为单纯DBI组的 (2 8 6 % ) 2倍 ;单纯DBI 1h后脑含水量明显升高 ,2 4h达高峰 ,16 8h降至正常水平 ;DBI合并SBI后脑含水量除 1h组外 ,其余时间组均明显较同时间单纯DBI组高 ,峰值提前至 12h ,16 8h仍未恢复正常 ;单纯DBI 6h后皮层神经元明显损伤 ,12h达高峰 ,16 8h接近正常 ;DBI合并SBI组皮层神经元损伤数 12h后仍持续增加 ,2 4h达高峰 ,16 8h仍未恢复正常 .结论 此模型可以复制SBI的重要临床特征 ,对SBI的基础研究有很大价值 .

AIM To set up a new animal model to study the diffuse brain injury (DBI) with secondary brain insult (SBI) in rats. METHODS On the basis of Marmarou's DBI model, a secondary insult was produced by bilateral carotid occlusion for 30 minutes. Water contents in brain cortex were measured, and the damaged neurons in supraventricular cortex were measured after DBI and SBI in rats. RESULTS The morality rate of DBI with SBI was approximately doubled compared with that of DBI alone (54 8% vs 28 6%, P <0 05). The water contents increased significantly 1 hour after DBI alone, reached the maximum value 24 hours after injury, and came back to the normal level 7days after injury. However, the water contents of rats with DBI together with SBI was much higher than that of DBI alone at all time points after injury except 1 hour after injury( P <0 05). The peak value was at 12 hours after injury and the content was still significantly high 7 days after injury. Damaged neurons increased significantly at 6 hours after DBI and SBI ( P <0 05), but there was no statistical difference between DBI with SBI group and DBI alone group. The progression of neuronal damage in DBI alone was relatively static at 12 hours, however, there was a remarkable increase in the neuronal damage of DBI with SBI group. The damaged neurons of DBI with SBI reached the peak 24 hours after injury. The damaged neurons of DBI with SBI group are much more than that of DBI alone group( P <0 05). CONCLUSION This model can produce a SBI process with clinical characteristics and can be used to study the pathophysiological process of DBI coupled with SBI.