| Heart failure is the end-stage period of various kinds of heart disease. Its incidence is very high and the five-year survive rate is very similar to the serious disease of cancer. So that many investigators have been paying more attention on studying of heart failure mechanism and its protecting methods. Now many studies focused on the mechanism of heart developing from the initial injury to the end-stage heart failure. It is believed that the occurrence and progression of heart failure are correlated most closely with left ventricular remodeling despite the causation. However, the mechanism contributes to left ventricular remodeling in heart failure progression is unclear. The matrix metalloproteinases(MMPs) are an family of enzymes which contribute to extracellular matrix degradation. The MMPs and their tissue inhibitors co-regulate the metabolism of the extracellular matrix, and play an important role in the myocardial extracellular matrix and LV remodeling. Recent investigation has shown that matrix metalloproteinases(MMPs) which exist largely in a latent form in the normal myocardium can be activated and present regular change after myocardial infarction. There is conflication on what MMPs change regulation is and how long this change lasts after infarction. Whether there is a relationship between MMPs activity increase and ventricular remodeling, whether MMPs are involved in ventricular remodeling during late period. It has been demonstrated that angiotensin II type 1 (AT1) receptor blockade and the third generation β-blockade can prevent LV remodeling and improve the prognosis of heart failure effectively, and it also found that AT1 receptor blockade affects collagen deposition and MMPs activity. Whether the third generation β-blockade affect collagen deposition and MMPs activity remain unknow. The aim of this study is to investigate the role of MMPs activity change and the relation between MMPs and heart function, to find out the effect ofβ-blockade and angiotensin II type 1 (AT1)receptor antagonist on MMPs activity and heart function after myocardial infarction. We designed this study in order to take more information for the mechanisms of CHD heart failure.Methods: The rats were developed into acute myocardial infarction by ligation of the left anterior descending coronary artery and divided into five groups of 1, 3 , 7, 14 and 42 days after infarction.There were five sham control groups corresponding to five infarcted groups. The following parameters were observed. 1,Measureing the MMPs activity in LV myocardium by zymography. 2, Monitoring the hemodynamic parameters by type MPA-V physiologic instrument. 3, Measuring the LV structure and function parameters by echocardiography. Another infarcted rats were devided into three groups and treated with Carvedilol, Losartan, placebo respectively at the day 1 after operation. The treatment lasted for 42 days, Measureing the parameters as above,and detecting the collagen concentration by Chloramine T method.Then comparing the parameters with placebo group.Results: MMP-1 and MMP-2 activity in LV myocardium increased and presented a dynamic change after infarction. Comparing with the sham control , MMP-1 and MMP-2 increased at day 1 (2.5-fold and 2 fold increase), at day 3 (4.5-fold and 4-fold increase ), peaked at day 7 (6.5-fold and 7.2-fold increase ), and declined thereafter at day 14 (2-fold increase ) and day 42 (1.5-fold increase ).MMP-1 activity in MI rats treated with carvedilol reduced by 35%±2.6%, MMP-2 activity reduced by 30%±2%. MMP-1 activity in MI rats treated with losartan reduced by 38%±2.6%, MMP-2 activity reduced by 32%±2%. Comparing with the sham control, LVEDP in AMI groups increased while dp/dtmax decreased significantly after infarction (P<0.01), and presented a dynamic change. LVEDP increased and dp/dtmax decreased significantly in day 42 group comparing with day 1 group after infarction ( 24.5±4.4 vs13.5±2.6mmHg, P<0.01, 3654±201 vs 4968±523 mmHg/s,P<0.01). LVEDP decreased and dp/dtmax increased significant...
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