摘要
目的 用阿霉素复制扩张型心肌病 (DCM )动物模型。方法 阿霉素 (每次 1mg/kg ,每周 2次 ,连续 8周 )耳缘静脉注射造成兔扩张型心肌病模型 ,观察实验组兔造模前后超声心动图的改变 ,用药结束后第 3周比较对照组和实验组动物心肌组织形态学改变。结果 超声心动图提示与造模前相比 ,实验组兔造模后左室收缩末期容积 (ESV) ,舒张末期容积 (EDV) ,左室收缩末期内径 (SD) ,舒张末期内径(DD)均明显增加 (P <0 0 1) ,射血分数 (EF)和心率 (HR)均明显降低 (P <0 0 1) ;实验组动物心肌组织形态学的改变也符合扩张型心肌病的病理学改变。结论 用阿霉素可成功复制出兔扩张心肌病模型。该模型不仅适合研究心肌超微结构改变及病理生理变化 ,也可用来评价心血管药物及其他治疗措施的疗效。
Objectives To establish a rabbit model of adriamycin-induced dilated cardiomyopathy. Methods Animals were randomly divided into 2 groups. Adriamycin was administered at a dose of 1 mg/kg intravenously twice a week for 8 weeks to the exeriment group. Transthoracic echocardiography was performed in the experiment group rabbits at baseline and additionally at 11 weeks after beginning of adria-mycin therapy to measure left ventricular dimensions and calculate ejection fraction. At 11 weeks, left ventricular slices of two group animals were processed for histologica(hematoxylin-eosin) staining. Results Transthoracic echocardiography provided adequate visualiztion of left ventricular dimensions and cardiac function. Compared to baseline, end-systolic volume increased from (0.61±0.15) mL to (1.18±0.34) mL(P<0.01), end-diastolic volume increased from (2.27±0.65) mL to (3.54±0.72) mL(P<0.01), end-systolic diameters increased from (6.4±1.3) mm to (8.7±1.6) mm(P<0.01), end-diastolic diameters increased from (10.2±1.8) mm to (13.4±2.1) mm(P<0.01), and heart rate decreased from (257±16) bpm/min to (215±21) bpm/min(P<0.01), ejection fraction decreased from 76.4%±6.9% to 59.2%±8.7%(P<0.01). Pathological examination demonstrated that compared with the control group, the cardiac muscular tissue of the experiment group were harmed, which characteristic were consistented with dilated cardiomyopathy in the human patients. Conclusions Chronic administration of intravenous adriamycin(1 mg/kg twice weekly for 8 weeks) to rabbits results in a dilated cardiomyopathy, which closely resembles the human condition and thus offers considerable potential for investigating the pathophysiology, pathogenic factors and newer therapeutic modalities.
出处
《岭南心血管病杂志》
2004年第1期54-56,共3页
South China Journal of Cardiovascular Diseases
