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纸质出版日期:2012
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李春, 王勇, 欧阳雨林, 等. 益心解毒方改善心梗后心衰大鼠心功能的作用研究[J]. 中国实验方剂学杂志, 2012,18(13):165-168.
LI Chun, WANG Yong, OUYANG Yu-lin, et al. Study on Effect of Yixin Jiedu Formula on Heart Failure after Myocardial Infarction in Rats[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(13): 165-168.
李春, 王勇, 欧阳雨林, 等. 益心解毒方改善心梗后心衰大鼠心功能的作用研究[J]. 中国实验方剂学杂志, 2012,18(13):165-168. DOI:
LI Chun, WANG Yong, OUYANG Yu-lin, et al. Study on Effect of Yixin Jiedu Formula on Heart Failure after Myocardial Infarction in Rats[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(13): 165-168. DOI:
目的: 阐明益心解毒方对心梗后心衰大鼠心功能的影响及其相关机制。 方法: 利用左冠状动脉结扎术复制心梗后心衰大鼠模型
并在术后将动物随机分为模型组、益心解毒方高、低剂量组((18.66
9.33 g·kg-1))和福辛普利钠组(4.67 mg·kg-1)
同时设立假手术组对照。术后第2天开始ig给药
连续给药28 d。通过心脏超声对各组动物的心功能做出评价;并留取各组动物血浆
通过放射免疫法对各组动物血浆中的醛固酮(ALD)和血管紧张素Ⅱ(AngⅡ)进行测定。通过免疫比浊法对血清中高敏C反应蛋白(hs-CRP)进行测定。 结果: 与假手术组相比
模型组大鼠的左室舒张末内径(LVEDd)和左室收缩末内径(LVEDs)显著增加(P<0.05)
射血分数(EF)和短轴缩短率(FS)明显下降(P<0.05);益心解毒方高、低剂量组以及福辛普利钠组均能提高心衰大鼠的EF和FS
同时益心解毒方能有效改善大鼠心功能并且缩短LVEDd和LVEDs。模型组大鼠的血浆Ang Ⅱ明显高于假手术组;益心解毒方高、低剂量以及福辛普利钠能够下调心衰大鼠血浆AngⅡ浓度
分别下调了16.58%
15.58%
12.79%(P<0.05)。益心解毒方能够有效的降低心梗后心衰大鼠血清中上升的hs-CRP水平
具有一定的抗炎作用。结论 益心解毒方能够缩短心衰大鼠的LVEDd和LVEDs进而改善心肌重塑的进展
提高心衰大鼠的心功能。其机制可能与降低心衰大鼠血浆中RAAS系统激活的水平尤其是AngⅡ水平
改善心脏的后负荷以及抗炎作用有关。
Objective: To clarify effect and possible mechanism of Yixin Jiedu formula (YXJDF) on the heart failure after infarction induced by Qi deficiency and blood stasis syndrome. Method: The heart failure model after myocardial infarction was prepared by left coronary artery ligation.Drugs were given by continuous intragastric administration for 28 d. Then cardiac function of each group was evaluated by echocardiography
plasma angiotensin Ⅱ (Ang Ⅱ) and aldosterone (ALD) levels were also examined by radioimmunoassay (RIA) in all groups. The level of high-sensitivity C-reactive protein (hs-CRP) in serum was detected by immunoturbidimetric assay. Result: Compared with the sham group
the left ventricular end-diastolic diameter (LVEDd) and left ventricular end-systolic diameter (LVEDs) of model group increased significantly (P<0.05)
ejection fraction (EF) and fractional shortening (FS) decreased significantly (P<0.05). After given the high-dose and middle-dose of YXJDF and the fosinopril sodium
the two drugs could improve EF and FS
further to improve the cardiac function. Moreover
YXJDF could effectively shorten the LVEDd and LVEDs
and fosinopril sodium did not work. RIA results showed that AngⅡof model group in plasma was significantly higher than sham group; the high-dose and middle-dose of YXJDF and fosinopril sodium could down-regulate the plasma AngⅡ by 16.58%
15.58%
12.79% (P<0.05) respectively. And the experimental results of immunoturbidimetric assay showed that YXJDF could reduce high levels of hs-CRP in serum and inhibit inflammatory response. Conclusion: YXJDF can shorten the LVEDd and LVEDs
and thus slow down the process of cardiac remodeling and strength the cardiac function. The mechanism may be that it can decrease plasma AngⅡlevels and reduce RAAS activity thus to improve cardiac afterload in heart failure rats and suppress the inflammatory response.
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