| Background:Acute myocardial infarction(AMI)is an acute and dangerous disease in coronary heart disease.In recent years,the incidence of AMI not only accounts for a large proportion of the elderly,but also gradually increases in the young adults.At present,with the continuous development of coronary intervention,more patients with AMI have achieved revascularization after coronary recanalization within effective time,avoiding heart pump failure caused by large areas of myocardial cell necrosis,contributing to the reduction of AMI mortality.However,after AMI,it can cause excessive activation of certain neuroendocrine hormones in the body,cause ventricular remodeling,and then cause myocardial contraction and diastolic dysfunction,even develop into heart failure(HF),which seriously threatens human health.Therefore,the effective prevention of ventricular remodeling has great significance for the prognosis of AMI patients.This article mainly explores the protective effect of Angiotensin Receptor Neprilysin Inhibitor(ARNI)on ischemic myocardium in AMI model rats,and clarifies the protective mechanism of ARNI on ischemic myocardium.Objective:1)To explore the protective effect of ARNI on ischemic myocardium in AMI rats.2)To verify whether ARNI can reverse ventricular remodeling after AMI.3)To compare the effect of ARNI and valsartan on the protective effect of ischemic myocardium.Methods:sixty male SD rats were randomly divided into Control group,MI group,MI-valsartan group,MI-ARNi group,15 rats in each group,ligating the left coronary anteriordescending artery to establish the rat model of myocardial infarction,the Control group only passed LAD without threading.Valsartan group and ARNI group were treated with valsartan(34mg / kg / day)and ARNI(68mg / kg / day)respectively for 3 hours after MI,6weeks in total.The Control group and MI group were given the same amount of normal saline.Serum NT-proBNP,hsTNT,aldosterone(ALD),and cGMP levels were measured at1 week,2 weeks,3 weeks,and 4 weeks.LVIDd,LVIDs,EF were measured by color Doppler echocardiography before and 6 weeks after treatment.After 6 weeks,the rats were sacrificed,the heart was removed and weighed,then myocardial tissue Masson staining was performed to calculate the collagen volume fraction(CVF).Results:1)The results of serum values in the same week showed that compared with the control group,serum NT-proBNP,hsTNT,ALD,cGMP levels in myocardial infarction group,valsartan group and ARNI group were significantly increased(P <0.05);compared with MI group,the serum NT-proBNP,hsTNT,ALD,and cGMP levels in the valsartan group and ARNI group were significantly reduced(P<0.05);compared with the valsartan group,the serum NT-proBNP,hsTNT,and ALD levels in the ARNI group were reduced,and the cGMP levels were increased,but no statistical significance(P>0.05).The levels of NT-proBNP,hsTNT,and ALD in the valsartan group and ARNI group decreased with the extension of treatment time.2)The results of cardiac ultrasound before treatment showed that compared with the control group,LVIDs was significantly increased,EF significantly reduced in the MI group,valsartan group and ARNI group(P<0.05).After 6 weeks of treatment,compared with the MI group,LVIDd and LVIDs in the ARNI group were significantly reduced,and EF was significantly increased(P<0.05);compared with the valsartan group,LVIDs was also significantly reduced in the ARNI group,and EF was further increased(P<0.05).3)The results of cardiac tissue weighing showed that compared with the control group,the left ventricular weight,right ventricular weight,and atrial weight were significantly increased in the MI group,valsartan group,and ARNI group(P<0.05);compared with theMI group,the left ventricular weight,right ventricular weight,and atrial weight were significantly reduced in the valsartan group and ARNI group(P<0.05);compared with the valsartan group,the left ventricular weight of the ARNI group was further reduced(P<0.05).4)Masson staining of myocardial tissue showed that compared with the control group,fibrosis was significantly changed and CVF was significantly increased in myocardial infarction group,valsartan group and ARNI group(P<0.05).Compared with MI group,the fibrosis was improved and the CVF was significantly reduced in the valsartan group and ARNI group(P<0.05);the fibrosis of the ARNI group was further improved and the CVF was reduced compared to the valsartan group(P<0.05).Conclusions:ARNI can improve the levels of NT-proBNP,hsTNT,ALD,and cGMP in rats with heart failure after AMI,reduce left ventricular volume,increase myocardial contractility,inhibit myocardial cell hypertrophy and fibrosis changes after AMI.It has protective effect on ischemic myocardium in rats with acute myocardial infarction. |
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