Abstract:

Abstract:Objective To observe the influence of  carvedilol in myocardial fibrosis in rats with heart failure after myocardial infarction and to explore the  mechanism of protective effect of carvedilol. Methods The left anterior descending coronary arteries of Wistar rats were  ligated to establish  rat models of heart failure. 32 rat heart failure models were established successfully after 6 weeks.32 rats with heart failure were divided into sham operation group(n=8),model group(n=8),model+low dose of carvedilol group(n=8),and model+high dose of carvediol group(n=8).The rats in model+low or high doses of carvedilol groups were  treated with carvediol in  low or high  doses (1 and 10 mg/kg carvediol) for 7 weeks  after the operation.The rats in sham operation and model groups were treated with 0.5% CMC-Na 10 mL?kg-1?d-1.All treatment regimens were initiated 6 weeks after operation and continued for 5 weeks.The activity of serum superoxide dismutase(SOD) was detected by xanthine oxidase method and the concentration  of serum malondialdehyde(MDA) was  detected by thiobarbituric acid method; the level  of serum BNP was detected by ELISA method;after Masson staining,the myocardial fibrosis of these rats were observed under light microscope.Results Compared with sham operation group,the serum BNP level and MDA concentration were increased(P<0.05) and the activity of SOD was decreased of the rats in the other groups; compared with  model group,the concentrations  of  serum MDA were decreased  and the activities of SOD were increased  significantly of the  in rats in model +low or high doses of carvedilol groups (P<0.01); the degree of myocardial fibrosis was reduced.Compared with model + low dose of carvedilol group,the serum BNP level was decreased(P<0.05),the concentration of  MDA  was decreased (P<0.05),and the SOD activity  was increased (P<0.05) of the  rats in  model + high dose of  carvedilol　group; the degree of  myocardial fibrosis was reduced.Conclusion Different doses  of  carvedilol can protect the myocardium  tissue and reduce the degree of  myocardial infarction;its mechanism may be related to  decreasing the concentration of serum MDA and  increasing the activity of serum SOD of the rats with heart failure.