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本实验通过腹腔注射阿霉素复制阿霉素心衰大鼠模型 ,以心功能及心肌细胞Ca ATPase活性为观察指标 ,研究中药心复康口服液对阿霉素心衰模型大鼠心功能及心肌Ca ATPase活性的影响。结果显示 :阿霉素模型组CO、±dp/dtmax分别为 2 9± 7.75ml/min ,4.38± 0 .43mmHg/s和 3.5 1± 0 .5 4mmHg/s ,与正常对照组比较P <0 .0 1;心复康口服液治疗组明显提高阿霉素心衰大鼠心脏CO(4 0 .0 5± 12 .5 7ml/min)、±dp/dtmax(5 .18± 0 .77mmHg/s ,4.35± 0 .71mmHg/s)值 ,与模型组比较分别有显著性差异 (P <0 .0 5 )。电镜细胞化学观察发现 :阿霉素模型组心肌细胞Ca ATPase反应较弱 ,沉淀物在肌膜和线粒体膜上较多 ;心复康口服液治疗组心肌细胞Ca ATPase反应较正常对照组、阿霉素模型组增强 ,反应物广泛分布于肌纤维膜、线粒体膜及肌浆网膜各处 ,呈细小园颗粒状 ,几乎连成线状围绕上述生物膜分布。提示心复康口服液可显著改善阿霉素心衰模型大鼠的心脏收缩和舒张功能。其机制可能是通过提高Ca ATPase活性 ,促进Ca2 +转运 ,防止心肌细胞Ca2 +超载。
In this experiment, adriamycin-induced heart failure rat models were replicated by intraperitoneal injection of adriamycin. Cardiac function and Ca ATPase activity in cardiomyocytes were used as observation indexes to study the cardiac function of Chinese medicine Xinfukang oral liquid in rats with adriamycin-induced heart failure. The effect of myocardial Ca ATPase activity. The results showed that the CO and ±dp/dtmax in the adriamycin model group were 29 ± 7.75 ml/min, 4.38 ± 0.43 mmHg/s, and 3.5 1 ± 0.54 mmHg/s, respectively, compared with the normal control group P <0. .0 1; Xinfukang oral liquid treatment group significantly improved CO heart rate in rats with adriamycin-induced heart failure (40.05±12.75ml/min), ±dp/dtmax (5.18±0.77mmHg/g s, 4.35 ± 0.71mmHg / s) value, compared with the model group were significantly different (P <0. 0 5). Electron microscopy revealed that Ca(superscript 2+)-ATPase in cardiomyocytes of adriamycin-treated model group was weaker than that in the control group. There were more deposits on the sarcolemma and mitochondrial membranes; the Ca ATPase response of cardiomyocytes in Xinfukang oral liquid-treated group was higher than that of the normal control group. The model group was enhanced, and the reactants were widely distributed in the myofiber membrane, mitochondrial membrane, and sarcoplasmic reticulum. The particles were fine granular and distributed almost linearly around the biofilm. Tips Xinfukang oral liquid can significantly improve cardiac contractility and diastolic function in adriamycin-induced heart failure model rats. The mechanism may be through increasing Ca ATPase activity, promoting Ca2+ transport, and preventing myocardial cell Ca2+ overload.