大鼠颅脑外伤致多器官功能障碍综合征模型的建立

Establishment of a model of multiple organ dysfunction syndrome resulted by craniocerebral trauma in rats

目的建立符合临床实际、简便易行的颅脑外伤致多器官功能障碍综合征(MODS)模型。方法采用改进自由落体法建立颅脑外伤致MODS模型,48只Wistar大鼠随机分为正常对照组、假手术组、颅脑外伤不同时间后6个亚组(4,12,24,36,48,72h组),记录各时相点大鼠颅脑外伤后的症状、体征,检测外周血WBC、肝肾功能、心肌酶学改变。光镜下观察肺、小肠、肝和肾组织病理变化,依据全身炎症反应综合征(SIRS)和MODS的诊断标准判断SIRS和MODS的发生率。结果(1)假手术组与正常对照组相比,其呼吸、心率、体温及外周血WBC、ALT、AST、BUN、Cr、CK的差异无显著意义(P>0.05);颅脑外伤组的上述各项指标均高于正常对照组、假手术组(P<0.01),并且在24～36h变化最明显;(2)大鼠颅脑外伤后各时相点各脏器组织均有不同程度的炎性损害,颅脑外伤组在24～36h时相点的脏器病理变化最显著,在48h稍有减轻,72h时相点仍可见炎性损害;(3)颅脑外伤组SIRS的发生率为100%;MODS发生率为69.4%,病死率为38.9%。结论(1)采用大鼠改良自由落体法可成功建立颅脑外伤致MODS的实验动物模型;(2)颅脑外伤后存在重要脏器的炎性改变及SIRS,提示SIRS是颅脑外伤致MODS的病理学基础。

Objective To establish a model that not only imitate the clinical features of multiple organ dysfunction syndrome （MODS） resulted by cranioeerebral trauma, but also performedeasity. Methods Multiple organ dysfunction syndrome （MODS） was induced in rats by cranioeerebral trauma modified mode made by dropping weight. 48 Wister rats were randomly divided into 3 groups： the normal control group, the sham--operative group, and the craniocerebral trauma group including 4h, 12h, 24h, 36h, 48h and 72h six time points. Changes of symptoms and signs including temperature, heart rate and respiration of each group were recorded. The amount of WBC and function of liver and kidney were assayed. Pathological changes of lung, liver, intestines and kidney were recorded and pictures were taken through optical microscope. Incidences of SIRS （Systemic Inflammatory Response Syndrome） and MODS were diagnosed by their criteria. Results （1）There were no significant differences in temperature, heart rate and respiration, and the levels of WBC, ALT, AST, BUN, Cr and CK among the normal control group and the sham-- operative group （P 〉 0. 05）. The rats of the craniocerebral trauma group had higher temperature, heart rate, respiration, WBC, ALT, AST, BUN, Cr and CK than the normal control group and the sham--operative group （P 〈 0.01）, the changes were biggest in 24--36 hour point. （2）After craniocerebral trauma, there were various inflammatory lesions on the organ tissue at every time point. The organ had significantly pathological changes at 24-36 hour point, and the changes gradually decreased in 48 hour point in the eraniocerebral trauma group. And it still had inflammatory lesions at 72 hour point. （3）Incidences of SIRS, MODS and mortality were 100%, 69.4% and 38.9% after craniocerebral trauma, respectively. Conclusions （1）An experimental animal model of MODS can be established in rats successfully through modified craniocerebral trauma mode made by dropping weight. （2）Craniocerebral trauma can cause lung, liver, intestines, kidney inflammatory lesions and SIRS. This suggests that SIRS may be the pathological bases of MODS resulted by cranioeerebral trauma.