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本实验通过腹腔注射阿霉素复制阿霉素亚急性心肌损伤大鼠模型 ,以心功能及心肌组织中谷胱甘肽过氧化物酶 (GSH— Px)活性、丙二醛 (MDA)含量为观察指标 ,研究中药心复康口服液对大鼠阿霉素亚急性心肌损伤时心功能及自由基代谢的影响。结果显示 :阿霉素模型组 GSH— Px活性和 MDA含量分别为 5 1.5 9± 2 .72 μ/m in/mg和 0 .66±0 .4 68nm ol/mg· pr,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损伤心肌组织 GSH— Px活性(64 .77± 5 .112 ) ,降低 MDA含量 (0 .3 2 6± 0 .2 4 1) ,与模型组比较有非常显著性差异 (P<0 .0 1) ,接近正常对照组值。同时心功能测定发现阿霉素模型组 Co、± dp/dtmax分别为 2 9±7.75 ml/min,4 .3 8± 0 .4 3 mm Hg/s和 3 .5 1± 0 .5 4 m m Hg/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损伤心脏 CO (40 .0 5± 12 .5 7ml/min)、± dp/dtm ax(5 .18± 0 .77mm Hg/s,4 .3 5± 0 .71m m Hg/s)值 ,与模型组比较分别有显著性差异 (P<0 .0 5 )。提示心复康口服液可显著改善 ADR亚急性损伤大鼠的心脏收缩和舒张功能。
In this experiment, adriamycin-induced subacute myocardial injury in rats was induced by intraperitoneal injection of adriamycin. The activity of glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in cardiac function and myocardial tissue were observed. Objective To study the effect of Xinfukang oral liquid on heart function and free radical metabolism of rats with adriamycin-induced subacute myocardial injury. The results showed that GSH-Px activity and MDA content in the adriamycin model group were 51.5 9±2.72 μ/m in/mg and 0.66±0.48 nmol/mg·pr, respectively, compared with the normal control group. P<0.01; Xinfukang oral liquid treatment group significantly increased the myocardial GSH-Px activity (64.77±5.112), and decreased the MDA content (0.32±2.6). 1) Compared with the model group, there is a very significant difference (P < 0.01), close to the normal control group value. At the same time, cardiac function tests revealed that the Co and ± dp/dtmax in the adriamycin model group were 29 ± 7.75 ml/min, 438 ± 0.43 mm Hg/s, and 3.51 ± 0.54 mm, respectively. Hg/s, compared with normal control group, P<0.01; Xinfukang oral liquid treatment group significantly increased doxorubicin-induced cardiac CO (40.05±12.75 ml/min), ± dp/dtm ax (5.18 ± 0.77mm Hg/s, 4.33±0.71m m Hg/s) values were significantly different from those in the model group (P < 0.05). Tip Xinfukang oral liquid can significantly improve the systolic and diastolic function of ADR subacutely injured rats.