Effect of angiotensin receptor neprilysin inhibitor on ventricular remodeling after myocardial infarction in rats

• 作者: Jian An Qing-Bo Bao Xiao-Hong Li Yan-Qing Guo Ye Du
• 来源期刊: 海南医科大学学报（英文版）
• 年，卷（期）: 2020,（22）
• 所属期刊栏目: Original article
• 页码范围: 1-5
• 页数: 5页
• 语种: 英文

摘要

Objective: To investigate the effect of Angiotensin Receptor Neprilysin Inhibitor (ARNI) on ventricular remodeling after AMI in rats. Methods: Sixty male SD rats were randomly divided into Control group, AMI group, AMI-valsartan group, AMI-ARNI group,15 rats in each group, ligating the left coronary anterior descending artery to establish the rat model of AMI. Valsartan group and ARNI group were treated with valsartan (34mg / kg / day) and ARNi (68mg / kg / day) for 6 weeks, the Control group and AMI group were given the same amount of normal saline. LVIDd, LVIDs, EF were measured by color doppler echocardiography before and 6 weeks after treatment. After 6 weeks, the rats were sacrificed, the hearts were weighed, then myocardial tissue Masson staining was performed to calculate the collagen volume fraction (CVF). Results: compared with the control group, LVIDs increased significantly with the reduction of EF in the AMI group, valsartan group and ARNI group (P<0.05). After 6 weeks of treatment, compared with the AMI group, LVIDd and LVIDs both reduced significantly with the increase of EF in the ARNI group (P<0.05). Compared with the control group, the left ventricular weight, right ventricular weight and atrial weight all increased significantly in the AMI group, valsartan group, and ARNI group (P<0.05); compared with the AMI group, the left ventricular weight, right ventricular weight, atrial weight and CVF reduced significantly in the valsartan group and ARNI group (P<0.05); compared with the valsartan group, the left ventricular weight and CVF further reduced in the ARNI group. (P<0.05).Conclusions: ARNI has the effect of reversing ventricular remodeling after AMI in rats, which can reduce left ventricular volume, increase myocardial contractility, and inhibit myocardial cell hypertrophy and fibrosis.