目的：探讨加参方通过抑制血管紧张素Ⅱ（AngⅡ）改善心梗模型大鼠心室重构的相关机制。方法：结扎SD大鼠冠状动脉前降支，建立心肌梗死模型，随机分为加参方3 g组、加参方6 g组、氯沙坦组、模型组，另设假手术组。药物干预组在心梗发生24 h后灌胃给药，其中加参方3 g组和6 g组给药剂量分别为3 g生药·kg^-1·d^-1和6 g生药·kg^-1·d^-1；氯沙坦组给药剂量为10 mg·kg^-1·d^-1；假手术组和模型组给予相同体积蒸馏水灌胃。4周后观察大鼠左室收缩末期内径（LVESD）、左室舒张末期内径（LVEDD）、左室后壁厚度（PWT）、左室射血分数（LVEF）、左室短轴缩短率（LVFS）和左室重量指数（LVWI）；胶原蛋白的分布和含量；血浆脑钠肽（BNP）、心肌组织匀浆中AngⅡ的含量等指标变化。结果：大鼠心梗后4周，与模型组相比，加参方6 g剂量组能够明显缩小心肌梗死范围，显著降低LVWI，明显抑制LVEDD和LVESD的扩大，提高LVEF和LVFS（P<0.05）；在缺血危险区，与模型组比较，加参方能明显降低胶原蛋白的含量（P<0.05），该作用呈剂量依赖性；血浆BNP、心肌组织匀浆中AngⅡ含量也明显低于模型组（P<0.05）。结论：加参方能改善心梗模型大鼠心室重构，其相关机制与抑制AngⅡ、改善心梗后早期左室形态学的重构、改善心肌纤维化和心脏的收缩功能有关。

This study was aimed to observe the effect of Jia-Shen prescription (JSP) on angiotensin Ⅱ (AngⅡ) inhibition, ventricular remodeling in myocardial infarction (MI) rat model. The anterior descending coronary artery of Sprague-Dawley rat was ligated to establish the MI rat model. Rats were randomly divided into the 3 g JSP group, 6 g JSP group, losartan group, model group, and the sham-operation group. Intragastric administration of medication was given 24 h after MI. In the 3 g and 6 g JSP group, JSP was given at the dose of 3 g·kg^-1·day^-1 and 6 g·kg^-1day^-1, respectively. Losartan was given at the dose of 10 mg·kg^-1·day^-1 in the losartan group. Same volume of distilled water was given to the sham-operation and model group. Four weeks later, the left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), posterior wall thickness (PWT), left ventricular ejection fraction (LVEF), left ventricular fractional shorten (LVFS), left ventricular weight index (LVWI), the distribution and content of collagen, plasma brain natriuretic peptide (BNP) and the AngⅡ content in myocardial tissues homogenate were observed. The results showed that 4 weeks after MI, compared to the model group, 6 g PJP reduced myocardial infarct size, LVWI, LVEDD and LVESD, and enhanced LVEF and LVFS (P < 0.05). In ischemic regions, compared to the model group, JSP can obviously reduce the content of collagen (P < 0.05). This effect had dose-dependent relationship. Plasma BNP and AngⅡ content in myocardial tissues homogenate were also obviously lower than the model group (P < 0.05). It was concluded that JSP can improve the ventricular remodeling of MI rat model. Its action mechanism may be through the AngⅡ inhibition, in order to improve the early stage left ventricular morphological remodeling, myocardial fibrosis and cardiac contractile function.

国家自然科学基金委面上项目（81173410）：加参优化方通过TGF-β/Smads通路改善心梗后心室重构作用机制的研究，负责人：朱明军；河南省高校科技创新团队支持计划（13IRTSTHN012）：中西医结合防治心血管疾病，负责人：朱明军；河南省科技厅中医药防治心血管疾病创新型科技团队（C20130050）：中医药防治心衰，负责人：朱明军。