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代谢综合征/心肌梗死大鼠模型的建立
引用本文:朱冰坡,范利,曹剑,刘霖,王浩,李健. 代谢综合征/心肌梗死大鼠模型的建立[J]. 中国组织工程研究与临床康复, 2012, 16(2): 265-268. DOI: 10.3969/j.issn.1673-8225.2012.02.017
作者姓名:朱冰坡  范利  曹剑  刘霖  王浩  李健
作者单位:解放军总医院老年心血管一科,北京市,100853
基金项目:课题受解放军总医院苗圃基金
摘    要:背景:代谢综合征合并急性心肌梗死是目前临床研究的热点问题之一,但现今有关代谢综合征合并急性心肌梗死动物模型的报告罕见报道.目的:建立代谢综合征/左前降支心肌梗死大鼠模型.方法:将雄性SD大鼠给予高果糖饮食,喂养时间8周,建立代谢综合征模型.再将此模型大鼠结扎左冠状动脉前降支深部建立代谢综合征/心肌梗死大鼠模型.结果与结论:采用高果糖喂养后的大鼠出现了高血压、高三酰甘油以及胰岛素抵抗现象(P < 0.05).代谢综合征/心肌梗死大鼠模型建模成功率为70%;组织切片可见大量心肌细胞坏死,瘢痕形成;超声心动图显示代谢综合征/心肌梗死模型大鼠左室舒张末内径和收缩末内径显著增加(P < 0.05),射血分数和缩短分数显著减少(P < 0.05),有创血流动力学检查提示代谢综合征/心肌梗死大鼠左室收缩压、左心室压最大上升速率和左心室压最大下降速率均下降(P < 0.05),而左室舒张末期压和心率升高(P < 0.05).结果证实,采用高果糖喂养可以制作可靠的大鼠代谢综合征模型;采用结扎左前降支方法能成功建立代谢综合征大鼠的心肌梗死模型.

关 键 词:代谢综合征  心肌梗死  大鼠  动物模型  组织构建

Establishment of a rat model of myocardial infarction with metabolism syndrome
Zhu Bing-po,Fan Li,Cao Jian,Liu Lin,Wang Hao,Li Jian. Establishment of a rat model of myocardial infarction with metabolism syndrome[J]. Journal of Clinical Rehabilitative Tissue Engineering Research, 2012, 16(2): 265-268. DOI: 10.3969/j.issn.1673-8225.2012.02.017
Authors:Zhu Bing-po  Fan Li  Cao Jian  Liu Lin  Wang Hao  Li Jian
Affiliation:First Department of Geriatric Cardiology, Chinese PLA General Hospital, Beijing 100853, China
Abstract:BACKGROUND: Metabolic syndrome associated with acute myocardial infarction is currently a hot topic of clinical research, but to date there are few animal models of metabolic syndrome with acute myocardial infarction. OBJECTIVE: To establish a rat model of metabolism syndrome associated with myocardial infarction in left anterior descending artery. METHODS: Male SD rats were fed with high-fructose diet for 8 weeks to establish metabolism syndrome model. The left anterior descending artery of the model rats was ligaturing to construct a rat model of metabolic syndrome with acute myocardial infarction. RESULTS AND CONCLUSION: Rats developed hypertension, hypertriglyceridemia and insulin resistance after fed with high-fructose diet (P < 0.05). The success rate of model construction in rat model of myocardial infarction with metabolism syndrome was 70%. Tissue sections showed massive myocardial cell necrosis with scar forming. Echocardiogram showed that in rats of metabolic syndrome/myocardial infarction group, left ventricular end-diastolic diameter and end-systolic diameter increased significantly (P < 0.05); ejection fraction and fractional shortening decreased significantly (P < 0.05). Invasive hemodynamics examination showed that left ventricular systolic pressure, +dp/dtmax and -dp/dtmax decreased (P < 0.05), while the left ventricular end diastolic pressure and heart rate increased (P < 0.05). These findings confirm that a reliable rat model of metabolism syndrome is successfully established using high-fructose diet; the rat model of myocardial infarction is successfully established by ligaturing the left anterior descending artery in rats with metabolism syndrome.
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