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目的:探讨参附强心对腹主动脉缩窄慢性心衰大鼠(CHF)心肌细胞Bcl-2表达的影响及其抗心衰机制。方法:选用Wistar雄性大鼠行腹主动脉缩窄法制备CHF模型,按照体重随机分为模型对照组、卡托普利阳性对照组、参附强心(按生药量计)2.14,1.07,0.54 g.kg-1剂量组,术后灌胃给药8周。通过生物信号采集系统,经心室插管测定心室压力;描记肢体II导联心电图(EKG);观察神经内分泌激素、心肌细胞凋亡和Masson染色心肌纤维化,探讨参附强心对慢性心衰治疗作用机制。结果:本实验成功复制大鼠慢性心衰模型,与假手术对照组比较,模型对照组左室内压峰值(LVSP)、左心室内压最大上升速率(+dp/dtmax)、左心室内压最大下降速率(-dp/dtmax)明显降低(P<0.05或P<0.001),表明心室收缩功能降低;左心室舒张末压(LVEDP)明显升高(P<0.001),表明舒张功能不全;心电图显示ST段上抬(P<0.05),QRS时限延长(P<0.05);血浆血管紧张素II(AngII)和醛固酮(ALD)均明显升高(P<0.01,P<0.01);心肌HE染色可见心肌细胞病变;Bcl-2阳性表达下调(P<0.001),片状或小灶状纤维化病变。参附强心2.14 g.kg-1灌胃8周可明显改善心衰大鼠心室收缩功能,使+dp/dtmax,-dp/dtmax明显升高(P<0.01,P<0.05),改善心脏舒张功能,使LVEDP明显回落(P<0.001);改善心电图ST段的异常抬高(P<0.05);降低血浆AngII,ALD含量。HE染色可见参附强心对心肌细胞结构的改善,使着色均匀、排列规整。可上调心衰大鼠心肌中抗凋亡基因Bcl-2的表达,并能改善病变心肌纤维化程度,从而起到控制心衰病变发展的作用。结论:腹主动脉缩窄法可成功制备大鼠后负荷加重心衰模型。参附强心可有效改善心衰大鼠血流动力学、上调心肌Bcl-2表达,抑制心肌纤维化和心室重构。
Objective: To investigate the effect of Shenfu cardiac on the expression of Bcl-2 and its mechanism of anti-heart failure in athymic rats with chronic heart failure (CHF). Methods: The CHF model was made by abdominal aorta constriction in Wistar male rats. The CHF model was randomly divided into model control group, captopril positive control group and Shenfu Qiangxin (according to crude drug amount) 2.14,1.07,0.54 g.kg-1 dose group, after intragastric administration for 8 weeks. Ventricular pressure was measured by ventricular intubation through biosignal acquisition system. Electrocardiogram (EKG) of limb II was recorded. Neuroendocrine hormones, cardiomyocyte apoptosis and Masson staining of myocardial fibrosis were observed, and the effect of Shenfu cardiac on chronic heart failure Mechanism. Results: The model of chronic heart failure was successfully replicated in this study. Compared with the sham operation control group, LVSP, + dp / dtmax and left ventricular pressure were the highest in the model control group (-dp / dtmax) decreased significantly (P <0.05 or P <0.001), indicating decreased ventricular systolic function; left ventricular end diastolic pressure (LVEDP) was significantly increased (P <0.001), indicating diastolic dysfunction; electrocardiogram ST segment elevation (P <0.05), prolonged QRS duration (P <0.05), and plasma levels of angiotensin II (AngII) and aldosterone (ALD) were significantly higher (P <0.01, P <0.01) Myocardial cell lesions; Bcl-2 positive expression was down (P <0.001), flaky or small focal fibrosis. The concentration of + dp / dtmax and -dp / dtmax increased obviously (P <0.01, P <0.05), and the heart was improved by gavage of 2.14 g.kg-1 for 8 weeks Diastolic function, LVEDP significantly decreased (P <0.001); improved ST segment abnormal elevation (P <0.05); decreased plasma AngII, ALD content. HE staining shows Shenfu cardiac function on myocardial cell structure, so that uniform coloring, arranged in a regular manner. Can upregulate the expression of anti-apoptotic gene Bcl-2 in the heart of rat with heart failure, and can improve the degree of myocardial fibrosis, thus play a role in controlling the development of heart failure. Conclusion: Abdominal aorta stenosis can be successfully prepared in rats with post-stress aggravating heart failure model. Shenfu Qinshen can effectively improve the hemodynamics of heart failure rats, upregulate the expression of Bcl-2 in myocardium, and inhibit myocardial fibrosis and ventricular remodeling.