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阿霉素诱导非缺血性心肌病模型小鼠方法的建立及其可行性评价 被引量:2

Establishment of Doxorubicin-induced Non-ischemic Cardiomyopathy Mice Model and Its Feasibility Evaluation
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摘要 目的:建立阿霉素诱导非缺血性心肌病模型小鼠的方法,并采用高频率超声心动图评价其可行性。方法:将小鼠随机分为对照组(生理盐水)和给药组(20mg·kg-1阿霉素),各39只,测量正常超声参数后一次性腹腔注射给药,每天监测心率,第3、4、5天行超声心动图检测,并在第5天后处死小鼠进行心肌病理学评价。结果:与对照组比较,给药组心率(P<0.05或P<0.01)、左室短轴缩短率(第5天,P<0.05)和每分钟输出量(第4、5天,P<0.05)均降低,对照组、给药组的病理评分中位数分别为0、2.5。结论:阿霉素短时间内能在小鼠上诱导出非缺血性心肌病模型,该模型具有经济、可靠、省时等优点,使用高频率超声心动图评价该模型建立成功。 OBJECTIVE: To establish doxorubicin-induced non-ischemic cardiomyopathy mice model and to evaluate feasibility of it by high frequency ultrasonic echocardiogram. METHODS: 78 mice were randomized into control group (normal saline, n=39) and administration group (20 mg·kg-1 doxorubicin, n=39). Conventional echocardiographic paramter was measured, and then both groups were given intraperitoneal injection. Heart rates of all mice were monitored every day. Ultrasonic echocardiography was carried out on the third, forth and fifth day. 5 days later all mice were sacrificed and myocardial pathology evaluation was performed. RESULTS: Compared with control group, the heart rate (P〈0.05 or P〈0.01), fractional shortening rate (on the fifth day, P〈0.05) and left vascular cardiac output per minute (on the forth and fifth day, P〈0.05) in administration group were all decreased. Medium pathologic scores were 0 for control group and 2.5 for administration group. CONCLUSIONS: Doxorubicin can be used to induce non-ischemic cardiomyopathy mice model. Established model is economical, reliable and time-saving. Results of high frequency ultrasonic echocardiogram shows established model is feasible.
出处 《中国药房》 CAS CSCD 北大核心 2010年第37期3477-3479,共3页 China Pharmacy
关键词 阿霉素 小鼠 心肌病模型 超声心动图 心功能 Doxorubicin Mice Cardiomyopathy model Ultrasonic echocardiogram Heart function
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参考文献10

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共引文献16

同被引文献20

  • 1黄伟哲,肖大伟,张保亭,宋银子,庞雅轩,杨默.比较麻醉和清醒状态对高频超声心动图评价小鼠心功能影响的研究[J].中华超声影像学杂志,2006,15(2):128-131. 被引量:11
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  • 10SUNG R, STEPHENS M, BLAYNEY L, et al. Cardiac hypertrophy and its regression in rat: comparison of morphological changes in response to aortic constriction, iron deficiency anaemia and isoprenaline [ J ]. J Mol Cell Cardiol, 1982, 14(9): 501-512.

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