中文摘要：

Yi-Qi-Fu-Mai（YQFM） is extensively used clinically to treat cardiovascular diseases in China. To explore the anti-hypoxia effect of the extract of YQFM preparation（EYQFM）, the EYQFM（1.4, 2.8, and 5.5 g·kg-1·d-1） was assessed for its heart-protective effect in a chronic intermittent hypoxia（CIH） animal model（oxygen pressure 7%-8%, 20 min per day） for 28 days of treatment. Betaloc(0.151 6 g·kg-1·d-1) was used as a positive control. The histopathological analyses of heart in CIH mice were conducted. Several cardiac state parameters, such as left ventricular ejection fractions（EF）, stroke volume（SV）, expression of creatine kinase（CK）, lactate dehydrogenase（LDH）, superoxide dismutase（SOD）, and malondialdehyde（MDA） were measured. The results showed that treatment with EYQFM markedly reversed swelling of the endothelial cells and vacuolization in the heart when compared with the model group. Further study demonstrated that EYQFM significantly improved ventricular myocardial contractility by increasing EF and SV. In addition, EYQFM inhibited the activity of CK, LDH, decreased the level of MDA and improved SOD activity. The results demonstrated that EYQFM significantly improved the tolerability of myocardium to hypoxia and ameliorated the cardiac damage in the CIH model.

英文摘要：

Yi-Qi-Fu-Mai（YQFM） is extensively used clinically to treat cardiovascular diseases in China. To explore the anti-hypoxia effect of the extract of YQFM preparation（EYQFM）, the EYQFM（1.4, 2.8, and 5.5 g·kg-1·d-1） was assessed for its heart-protective effect in a chronic intermittent hypoxia（CIH） animal model（oxygen pressure 7%-8%, 20 min per day） for 28 days of treatment. Betaloc（0.151 6 g·kg-1·d-1） was used as a positive control. The histopathological analyses of heart in CIH mice were conducted. Several cardiac state parameters, such as left ventricular ejection fractions（EF）, stroke volume（SV）, expression of creatine kinase（CK）, lactate dehydrogenase（LDH）, superoxide dismutase（SOD）, and malondialdehyde（MDA） were measured. The results showed that treatment with EYQFM markedly reversed swelling of the endothelial cells and vacuolization in the heart when compared with the model group. Further study demonstrated that EYQFM significantly improved ventricular myocardial contractility by increasing EF and SV. In addition, EYQFM inhibited the activity of CK, LDH, decreased the level of MDA and improved SOD activity. The results demonstrated that EYQFM significantly improved the tolerability of myocardium to hypoxia and ameliorated the cardiac damage in the CIH model.