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大鼠胸主动脉缩窄诱导心肌肥厚模型的建立
引用本文:周亚光,屠恩远,王照华,杨光田.大鼠胸主动脉缩窄诱导心肌肥厚模型的建立[J].中国实验动物学杂志,2008(12):21-24.
作者姓名:周亚光  屠恩远  王照华  杨光田
作者单位:华中科技大学同济医学院附属同济医院急诊内科,武汉430030
基金项目:国家自然科学基金资助项目(30500657).
摘    要:目的建立大鼠胸主动脉部分缩窄诱导心肌肥厚动物模型。方法雄性SD大鼠30只,随机分为两组:胸主动脉缩窄组20只和同期假手术组10只。在右无名动脉和左颈总动脉之间将主动脉结扎于8G针头上,随后将针头退出即可。术后10周,采用超声心动图检测心脏、观察心脏的大体剖面以及HE染色、测量心肌肥厚指数评价心肌肥厚的效果。结果术后10周,肉眼观:模型组心脏体积明显大于对照组。M型超声示:模型组较假手术组缩短分数下降,左室内径和室壁厚度明显增加。超声测量结果示:模型组与假手术组比较:室间隔厚度增加明显(2.527±0.269 vs.1.943±0.1)mm,(P〈0.01);后壁厚度增加明显(2.492±0.242 vs.1.902±0.076)mm,(P〈0.01);缩短分数略减小(49±7.681 vs.55.7±9.828)(P〉0.05);左室舒张末期内径、左室收缩末期内径及射血分数均无明显变化。心脏肥厚指数明显增大(3.196±0.11 vs.1.785±0.099),P〈0.01。结论胸主动脉缩窄可以导致大鼠心肌肥厚,为研究心室肥厚、心肌功能障碍以及心肌重构提供了一个很好的模型。

关 键 词:胸主动脉部分缩窄  心肌肥厚  模型  动物

Thoracic Aorta Constriction-Induced Cardiac Hypertrophy Model in Rats
ZHOU Ya-guang,TU En-yuan,WANG Zhao-hua,YANG Guang-tian.Thoracic Aorta Constriction-Induced Cardiac Hypertrophy Model in Rats[J].Chinese Journal of Laboratory Animal Science,2008(12):21-24.
Authors:ZHOU Ya-guang  TU En-yuan  WANG Zhao-hua  YANG Guang-tian
Institution:(Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China)
Abstract:Objective To establish a cardiac hypertrophy model by partial ligation of thoracic aorta in rats. Methods Thirty male Sprague Dawley (SD) rats were randomly divided into sham surgery ( n = 10) and operation ( n = 20) groups. Operation methods: The suture was snugly tied around the 22-gauge needle on the aorta between the origin of the right innominate and left common carotid arteries. After ligation, the needle was quickly removed. Echoeardiography, the external appearance and HE staining of myocardial samples were performed 10 weeks after the surgery. Results After 10 weeks, the volume of heart in operated rats is increased than that of sham-operation groups. Compared with the sham-operated rats, M-mode USG demonstrated that the left ventricle (LV) cavity and the posterior wall thickness in the rats of operated groups were markedly increased and its fractional shortening decreased. Compared with the sham-operation group, the operated rats showed that the interventricular septum thickness (2. 527 ± 0. 269 vs. 1.943 ±0.1 mm, P 〈 0.01 ), and the posterior wall thickness (2.492 ± 0. 242 vs. 1.902 ±0.076 mm, P〈 0.01) increased; the fractional shortening diminished (4.9 ± 7.681 vs. 55.7 ±9.828 mm, P 〉 0.05) ; the cardiac hypertrophy index increased (3. 196 ±0.11 vs. 1.785 ± 0.099 mm, P 〈 0.01 ) ; the changes of LV internal diastolic dimension (LVIDd), LV internal systolic dimension (LVIDs) and ejection fraction were not significant. Conclusion Thoracic aorta constriction (TAC) induced rat cardiac hypertrophy will provide a reproducible model useful for study of cardiac hypertrophy, myocardial dysfunction and myocardial remodeling.
Keywords:Thoracic aorta constriction (TAC)  Cardiac hypertrophy  Disease model  Rat
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