| Background: BNP, secreted from the ventricular myocardium, reflecting the ventricular stress, will elevate in cardiac dysfunction patients' plasma. Many researches on ACEI and P blocker improving the cardiac remodeling of MI rat have been reported in the recent years. But the papers on how and when to use ACEI and 3 blocker will limit the infarction size and improve the cardiac remolding in this model were rarely reported. In present experiment we investigated these problem in the MI rat, Method: Acute experiment: 50 LAD ligation rats were randomized into three groups: metoprolol group, imidapril group and control group. The rats received metoprolol, imidapril or sterile water by gastric gavage for 6 days respectively, supplemented with two intraperitoneal doses over the first 24 hours. The rats without LAD ligation were put into the sham-operated group. 7 days after operation, echocardiography was performed and the plasma BNP & ET-1 were determined in the abdominal artery blood.Chronic experiment: 48 hours after the operation, 96 LAD ligation rats were randomized into three groups: metoprolol group, imidapril group, control group. Then, the rats received metoprolol, imidapril or sterile water by mouth, which had been dissolved in drinking water, sham-operated group was set. 4 weeks after operation, echocardiography was performed, and plasma BNP and ET-1 were determined in the abdominal artery blood. The acute and chronic experiment groups' hearts were fixed in the 10% formalin for two weeks, then the pathological stain was done and the infarction size was measured. Results:1. Acute experiment: In comparison with that of control group, imidapril significantly limited the infarction size (P<0.05), while themetoprolol didn' t appear this kind of effect. Compared with that ofthe imidapril group, the control group' s left ventricular relativeweight significant decreased (P<0. 05), While that of metoprolol grouphad no significant difference with the other groups (P>0. 05). In theaspect of the right ventricular relative weight, the ventricularrelative weight, right/left ventricular weight, there was nosignificant difference between the three AMI groups. Compared withthat of the control groups, metoprolol treatment didn' t limit theaugmentation of LVESD and LVEDD (P>0. 05), while imidapril treatmentsignificantly limited the increment of LVESD and LVEDD(P<0.001). Incomparison with that of control group, the treatment with metoprololor imidapril significantly decreased the plasma BNP (P=0. 047, P<0. 001),while the imidapril treatment decreased the plasma BNP greater thanthat of metoprolol group (P<0. 001). Compared with that of the controlgroup, the metoprolol treatment didn' t significantly decrease theLAD. While the imidapril treatment significantly limited theincrement of LAD, and decreased the incidence of LA thrombosis.2. Chronic experiment: Compared with that of the control group, thedose-increasing metoprolol treatment and imidapril treatmentsignificantly limited the increment of LV relative weight, RV relativeweight, right /left ventricular weight, ventricular relative weight,LVESD, LVEDD, LAD, plasma BNP and plasma ET-1 (P<0.01).Conclusion: 1. imidapril used in early stage after myocardial infarctioncan limit the myocardial infarction size and improve the early stage ofcardiac remodeling, while metoprolol can' t be found have this kind ofeffect. 2. the treatment of imidapril and dose-increasing metoprolol canimprove cardiac remodeling and decrease the plasma BNP & ET-1 after acutemyocardial infarction. 3. when and how to use the metoprolol will influencethe cardiac remodeling differently. |