参芪扶心口服液对心肌梗死后左心衰大鼠血浆利钾尿肽与心脏重塑的影响

 目的观察参芪扶心口服液对实验性心肌梗死(心梗)后心力衰竭(心衰)大鼠血浆利钾尿肽(KP)、左室舒缩功能及左室重塑的影响。方法结扎大鼠左冠状动脉前降支制作急性心肌梗死后心衰模型,左心室插管术测定血液动力学指标;放免法测定血浆KP,心钠素(ANP),血管紧张素Ⅱ(AngⅡ)及内皮素-1(ET-1)浓度,并观察心脏形态学结构及胶原成分、心脏质量/体质量(HM/BM)、左心腔面积(LVA)、单位面积内心肌细胞核数(MNN)的变化。结果与模型组相比,高剂量(15g·kg^-1)组等容收缩未期心肌缩短最大速度(V_max)、左心室舒张期压力下降最大变化速率(-dp/dt_max)及左心室内压峰值(LVSP)增加;左心室舒张末压(LVEDP)降低;血浆KP,AngⅡ及ET-1浓度降低,均有显著性差异(P<0.05或P<0.01)。心肌细胞周围胶原组织明显减少,心脏质量/体质量心脏比值变小、单位面积内MNN明显增多、LVA明显缩小(P<0.05或P<0.01)。中剂量组(10g·kg^-1)、低剂量组(5g·kg^-1)血浆ANP水平下降明显(P<0.01)。结论参芪扶心口服液能改善心梗后心衰大鼠左室舒缩功能,降低KP,AngⅡ,ET-1浓度,影响ANP分泌,有一定抑制左室重塑的作用。

Effects of Shenqi Fuxin oral liquid on plasma kaliuretic peptide, myocardial contractility and relaxation of left ventricle and left ventricular remodeling in experimental rats with heart failure after myocardial infarction

OBJECTIVE To observe the effects of Shenqi Fuxin oral liquid(SQFXOL) on plasma kaliuretie peptide (KP), the left ventricular remodeling and the myocardial contractility and relaxation of left ventricle in experimental rats with heart failure(HF) after myocardial infarction. METHODS The hemodynamie parameters were measured by the method of the catheterization. Plasma concentrations of KP, ANP, AngⅡ and ET-1 were determined by radioimmunoassays. The changes of heart morphological structure, collagen element, heart mass/body mass ratio (HM/BM), left intraventrieular area (LVA) and myocardial nuclei number (MNN) per square area were compared. RESULTS In the mice treated with high dose(15 g·kg^-1), the LVSP,-dp/dt_max and V_max were increased, LVEDP was decreased, plasma concentrations of KP, AngⅡ and ET-1 were decreased significantly (P<0.05 or P<0.01). The collagen tissues around myocardial cells were reduced. HM/BM and LVA were lowered, and MNN per square area were increased (P<0.05 or P<0.01). The levels of plasma ANP in the mice treated with middle dose(10 g·kg^-1)and low dose(5 g·kg^-1) were significantly lower than those in model group (all P<0.01). CONCLUSION SQFXOL reduces the plasma concentrations of KP, AngⅡ, ET-1, and ANP, improves the myocardial contractility and relaxation of left ventricular and inhibites left ventricular remodeling in rats with HF after myocardial infarction.