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目的 :探讨阿霉素诱导兔心肌病模型的可行性 ,并利用经胸超声心动图进行评估。方法 :2 0只兔每周静脉注射阿霉素 2mg·kg-1,共计 8周 (总剂量 16mg·kg-1) ,另 8只每周注射同等剂量的生理盐水作为对照组。基础状态 (未注药前 )、12周时分别进行兔超声心动图检查 ,分别测量左室舒张期末、收缩期末内径 ,室间隔和左室后壁厚度 ,以及射血分数和短轴缩短率。 12周时阿霉素组和对照组分别取 2只进行心肌病理切片检查。结果 :阿霉素组与基础状态相比 ,12周时左室舒张期末内径显著扩大(10 .5± 1.3和 15 .8± 2 .1mm ,P <0 .0 5 ) ,收缩期末内径显著扩大 (8.7± 1.0和 10 .3± 1.1mm ,P <0 .0 5 ) ,射血分数显著降低 (6 3.4± 8.4和 38.8±7.6 ,P <0 .0 5 ) ,短轴缩短率显著降低 (P <0 .0 1) ,室间隔和左室后壁厚度无显著性变化 (37.6± 7.6和 2 1.2± 6 .7,P >0 .0 5 ) ;对照组左室舒张期末、收缩期末内径、室间隔和左室后壁厚度、射血分数和短周缩短率均无显著性变化 (P >0 .0 5 )。阿霉素组病理结果显示了与人类阿霉素心肌毒性相似的改变 ,心肌细胞变性、线粒体和肌浆网水肿、细胞内空泡增多。结论 :静脉注射阿霉素可以诱导形成非缺血性心肌病模型 ,结果可靠 ,成功率高。经胸超声心动图可以用来监测评估模型
Objective: To investigate the feasibility of doxorubicin-induced rabbit cardiomyopathy model and evaluate the effect of transthoracic echocardiography. METHODS: Twenty rabbits were intravenously injected with doxorubicin 2 mg · kg -1 every week for 8 weeks (total dose of 16 mg · kg -1), and the other 8 rabbits were injected weekly with the same dose of saline as the control group. Rabbit echocardiography was performed at the baseline (baseline) and at 12 weeks. The left ventricular end diastolic dimension, end systolic dimension, interventricular septum and left ventricular posterior wall thickness, ejection fraction and short axis shortening were measured. At 12 weeks, doxorubicin group and control group were taken 2 pathological examination. Results: Compared with the basal state, the end-diastolic diameter of the left ventricular end-diastolic dimension significantly increased at 10 weeks (10.5 ± 1.3 and 15.8 ± 2.1mm, P <0.05) in adriamycin group and significantly increased at the end of systole (8.7 ± 1.0 and 10.3 ± 1.1 mm, P <0.05). The ejection fraction decreased significantly (6 3.4 ± 8.4 vs 38.8 ± 7.6, P <0.05), and the short axis shortening rate was significantly reduced P <0.01), there was no significant change in the interventricular septum and left ventricular posterior wall thickness (37.6 ± 7.6 and 2 1.2 ± 6.7, P> 0.05); at the end of left ventricular diastolic phase, end systolic diameter , Ventricular septum and left ventricular posterior wall thickness, ejection fraction and shortening shortening rate had no significant change (P> 0.05). The doxorubicin group showed pathological changes similar to those of human doxorubicin with cardiomyocyte degeneration, mitochondria and sarcoplasmic reticulum edema and increased intracellular vacuolization. Conclusion: Intravenous doxorubicin induces the formation of non-ischemic cardiomyopathy model with reliable results and high success rate. Transthoracic echocardiography can be used to monitor the assessment model