改良法建立内膜损伤致大鼠颈动脉狭窄模型  

Establishment of model for carotid artery stenosis caused by intimal injury in rats by modified method

作　　者：张耀雷[1] 李昆[1] 张彦[2] 杨炯[2] 呼永和[3] 

机构地区：[1]成都军区总医院中心实验室,成都610083 [2]成都军区总医院心内科,成都610083 [3]成都军区总医院中医科,成都610083

出　　处：《西南国防医药》2016年第12期1409-1412,共4页Medical Journal of National Defending Forces in Southwest China

基　　金：全军医学科技"十二五"重点项目(BWS11J067)

摘　　要：目的改良球囊致内膜损伤建立大鼠颈动脉狭窄模型,并对其发生机制作初步探究。方法 42只SD大鼠随机分为模型组(n=21)和假手术组(n=21),模型组利用10 ml注射器针头模拟球囊抽拉致内膜损伤建立颈动脉狭窄模型;假手术组除针头抽拉损伤外,其余处理与模型组一致。伊文思蓝染色观察两组(每组3只)术侧颈总动脉内膜损伤差异;分别于术后1、2及3 w取两组颈总动脉(每组每次6只)行HE染色,观察血管狭窄变化;将2 w颈总动脉行α-smooth muscle actin免疫组化染色及二氧乙啶(DHE)测量活性氧(ROS)含量。结果伊文思蓝染色指示,针头抽拉区域内膜损伤。HE染色显示,模型组术后1 w时内膜开始增殖,2 w时内膜快速增殖达到1 w时的6.1倍,血管狭窄形成;3 w时内膜缓慢增值达到1 w时的6.8倍。α-smooth muscle actin染色指示新生内膜大部分为平滑肌细胞(VSMCs)。与假手术组相比,模型组ROS表达量急剧升高(P<0.01)。结论利用注射器针头抽拉成功建立大鼠颈动脉狭窄模型,其机制可能是内膜损伤使ROS含量升高,诱导VSMCs由中膜迁移至内膜并恶性增殖,从而导致颈动脉狭窄发生。Objective To establish a model for carotid artery stenosis caused by intimal injury in rats by modified method and to preliminarily explore the occurrence mechanism. Methods A total of 42 SD rats were randomly divided into two groups： the model group and the sham-operation group（n=21, respectively）. A model for carotid artery stenosis was established in the model group by use of a 10 ml syringe needle to simulate the intimal injury caused by balloon drawing; except for needle drawing injury, other treatments in the sham-operation group were the same as that in the model group. Evans blue stain was used to observe the difference in the common carotid artery injury on the operation side in the two groups （three rats in each group）; the cephalic artery in the two groups （six rats in each group） was sampled one, two and three weeks after the operation for HE stain to observe the change of angiostenosis; the two-week cephalic artery was received a-smooth muscle actin immunohistochemical staining and DHE to measure the content of ROS. Results Evans blue stain showed that intimal injury was caused in the needle drawing area. HE stain indicated that the intima began to increase within one week after the operation in the model group and increased to 6.1 times of that in one week upon two weeks, and angiostenosis is formed; the intima slowly increased to 6.8 times of that in one week upon three weeks, α-smooth muscle actin stain indicated that most of the new intima was VSMCs. Compared with the sham-operation group, the ROS in the model group increased greatly（P 〈 0.01）. Conclusion Carotid artery stenosis model in rats may be easily established by drawing of syringe needle. The mechanism may be that the intimal injury causes the increase of ROS, induces VSMCs to migrate from the media to the intima and proliferate malignantly, causing carotid artery stenosis.

关 键 词：注射器针头 颈动脉狭窄 大鼠模型 ROS 

分 类 号：R543.4[医药卫生—心血管疾病]