大鼠二次脑损伤模型的建立

目的　建立弥漫性脑损伤 (diffusebrianinjury ,DBI)合并缺血性二次脑损伤 (secondarybrianinsult ,SBI)大鼠模型。　方法　在Marmarou模型基础上结扎双侧颈总动脉 30min ,制成缺血性SBI模型 ,观察大鼠神经损伤严重程度评分 (NSS)、脑组织含水量及室上区皮层损伤神经元数改变。　结果　合并SBI组大鼠死亡率 ( 4 8.1 % )约为单纯DBI组 ( 2 6 .2 % )的 2倍 (P <0 .0 5) ;合并SBI组在损伤 2 4h后NSS明显高于单纯DBI组 (P <0 .0 5) ;单纯DBI 1h后脑含水量明显升高 ,于 2 4h达高峰 ,随后逐渐下降 ,1 6 8h降至正常 ,而合并SBI后除 1h组外 ,其余时间组脑含水量均明显高于同时间单纯DBI组 (P <0 .0 5) ,且峰值提前至 1 2h ,1 6 8h仍未恢复正常 ;单纯DBI 6h后皮层神经元明显损伤 (P <0 .0 5) ,1 2h达高峰 ,1 6 8h恢复正常 ,而合并SBI组神经元损伤数 1 2h后还增加 ,2 4h达高峰 ,1 6 8h仍未恢复正常 (P <0 .0 5)。　结论　此模型可以复制SBI的重要临床特征 ,对SBI的基础研究有重要价值。

Rat model of diffuse brain injury with secondary brain insult

Objective To set up a new rat model for studying diffuse brain injury (DBI) with ischemic secondary brain insult (SBI). Methods Fifteen minutes following the impact injury, a secondary insult was produced by occlusion of bilateral carotid for 30 minutes. The behavioral changes were evaluated by the neurological severe score (NSS). Water contents in brain cortex were measured and the damaged neurons in supraventricular cortex counted after the DBI and the SBI in rats. Results The mortality of DBI rats with SBI was double as much as that with DBI alone (48.1% vs 26.2%, P <0.05). The NSS of DBI rats with SBI is much higher than that of DBI rats alone 24 hours after injury ( P <0.05). The water contents were increased significantly one hour after DBI alone, reached the maximal value 24 hours after injury and returned to the normal level 168 hours after injury. However, the water contents of DBI rats with SBI were much higher than that of DBI rats alone at any time point after injury except for one hour after injury ( P <0.05). The peak value appeared at the 12th hour after injury and the content was still high significantly 168 hours after injury. The damaged neurons were increased significantly at the 6th hour after DBI and SBI ( P <0.05), reached the peak after 12 24 hours and returned to normal after 168 hours. The evolution of neuronal damage in DBI rats was relatively static at the 12th hour. However, there was a remarkable increase in the neuronal damage of SBI rats. The damaged neurons of DBI rats with SBI was increased gradually after 12 hours and reached the peak 24 72 hours after injury but did not return to normal at the 168th hour ( P <0.05). Conclusions This model can produce the SBI process similar to the clinical characteristics and is important for the study of the pathophysiological process of DBI complicated by SBI.