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动脉粥样硬化兔锁骨下动脉盗血模型的建立
引用本文:张桂运,陈左权,凌锋,李玉健,王岩,顾斌贤,吴春红,俞丽敏.动脉粥样硬化兔锁骨下动脉盗血模型的建立[J].中国脑血管病杂志,2009,6(7):355-358.
作者姓名:张桂运  陈左权  凌锋  李玉健  王岩  顾斌贤  吴春红  俞丽敏
作者单位:1. 同济大学附属同济医院神经外科,上海,200065
2. 首都医科大学附属宣武医院神经外科
摘    要:目的通过手术结扎或血管内栓塞技术,建立动脉粥样硬化兔锁骨下动脉盗血模型。方法取32只雄性新西兰大白兔(体质量3.0~3.5kg),随机分为普通饮食对照组、高脂饮食对照组、高脂饮食结扎组和高脂饮食栓塞组,每组8只。高脂饮食配方为89%基础饲料+1%胆固醇+5%蛋黄+5%猪油,持续喂养12周。确定动脉粥样硬化通过病理检查,显示高脂饮食兔的主动脉弓和颈总动脉分叉处动脉内膜明显增厚。通过结扎兔右侧锁骨下动脉或血管内栓塞左侧锁骨下动脉,模拟临床上由于动脉粥样硬化斑块形成导致的锁骨下动脉盗血患者的前、后循环血流动力学状态。结果①高脂饮食结扎组造模前循环时间长于普通饮食组,左侧椎动脉造影显示循环时间分别为(6.68±0.07)、(6.56±0.07)S,t=3.429,P〈0.01;但与高脂饮食组比较,差异无统计学意义(P〉0.05);造模后则长于普通饮食组,亦长于高脂饮食组,循环时间分别为(7.80±0.11)、(6.56±0.07)、(6.71±0.08)s,均P〈0.01。②右侧椎动脉造影显示高脂饮食栓塞组造模后,右侧椎动脉循环时间、普通饮食组及高脂饮食组循环时间分别为(7.83±0.10)、(6.60±0.08)、(6.75±0.05)S,均P〈0.01。结论该模型能够在某种程度上模拟临床动脉粥样硬化患者锁骨下动脉盗血时的脑血流动力学状态。

关 键 词:动脉粥样硬化  锁骨下动脉窃血综合征  模型,动物  

Establishment of a model of subclavian steal in atherosclerotic rabbits
ZHANG Gui-yun,CHEN Zuo-quan,LING Feng,LI Yu-jian,WANG Yan,GU Bin-xian,WU Chun-hong,YU Li-min.Establishment of a model of subclavian steal in atherosclerotic rabbits[J].Chinese Journal of Cerebrovascular Diseases,2009,6(7):355-358.
Authors:ZHANG Gui-yun  CHEN Zuo-quan  LING Feng  LI Yu-jian  WANG Yan  GU Bin-xian  WU Chun-hong  YU Li-min
Institution:.(Department of Neurosurgery, Tongji Hospital of Tongji University, Shanghai 200065, China)
Abstract:Objective To establish a subclavian steal rabbit model through surgical ligation or endovascular embolization techniques. Methods Thirty-two male New Zealand white rabbits weighing 3.0 to 3.5 kg were randomly assigned to normal diet control, high-fat diet control, high-fat diet plus ligation and high-fat diet plus embolizatiou groups (n = 8 in each group). The high-fat diet forage included 89% basic forage + 1% cholesterol + 5% yolk + 5% lard, and the rabbits were fed continuously for 12 weeks. Pathological examination showed significantly thickened intima at the bifurcation of the aortic arch and the carotid arteries in the high-fat diet rabbits, even plaques were formed. The state of unilateral subclavian steal were produced through ligation of right subclavian artery or endovascular embolization of left subclavian artery, and thus changed the pressure gradients between the anterior and posterior circulation, so as to mimic the hemodynamic state of the anterior and posterior circulation in patients with subclavian steal caused by atherosclerotic plaque formation in clinical practice. Results Before the model was made, the circulation time was longer in the high-fat diet ligation group 6. 68 ± 0. 07 s than that in the normal diet control group 6. 56 ±0.07 s(t = 3. 429, P 〈 0. 01 ) ; but there was no significant difference compared to the high-fat diet control group ( P 〉 0. 05 ) ; After the model was made, the circulation time was longer than that in both normal diet control and high-fat diet control groups, and they were 7. 80 ± 0. 11 s, 6. 56 ± 0. 07 s and 6. 71 ± 0. 08 s, respectively ( t = 26. 899, all P 〈 0. 01 ). The circulation time in the high-fat diet embolization group 7. 83 ± 0. 10 s was longer than that in both normal diet control 6. 60 ± 0. 08 s and high-fat diet control groups 6. 75 ± 0. 05 s, respectively (P 〈 0. 01 all). Conclusion This model may mimic the hemodynamic state at the time of subclavian steal in patients with atherosclerosis in clinical practice.
Keywords:Atherosclerosis  Subclavian steal syndrome  Model  animal  Rabbits
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