Change of cardiac matrix metalloproteinases during the progression of left ventricalar remodeling in a rat mod el of acute myocardial infarction

Objective To investigate the change of cardiac matrix metalloproteinases(MMPs) activities and the relationship of MMPs with ventricular remodeling and heart function during the progression of acute myocardial infarction (AMI) in a rat model. Methods 90 male Sprague Dawley rats were divided randomly into sham operated group and AMI group. AMI group rats were undergone acute myocardial infarction by ligation of the anterior descending coronary artery and divided randomly into five groups of 1, 7, 14, 28, and 42 days after infarction. Sham operated group rats were also randomized into five sham-operated groups corresponding to the five infarcted groups. Heart function and left ventricular remodeling were confirmed by echocardiography and hemodynamic measurements. MMPs activities were assessed by Zymography. Results Left ventricular end-diastolic diameter (LVEDD) increased gradually,and fractional shortening (FS) and left ventricular ejection fraction (LVEF) reduced from day 14 up to day 42 after the created myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) increased gradually, left ventricular (LV) pressure maximal rate of rise and fall (dp/dtmax and dp/dtmin) reduced from day 1 up to day 42 after rat acute myocardial infarction. MMP 2 and MMP 9 activities rose to peak at day 7 after infarction and decreased thereafter. MMP 2 and MMP 9 activities were significantly higher for each time point in the infarction rats than those in sham-operated ones (all P 0.01-). MMP 2 activity in the myocardium at day 7 after infarction was significantly correlated with LVEDD, FS, LVEF, and dp/dtmax ( r =0.92, -0.91, -0.88, -0.87,respectively; P 0.05-～0.01). There was significant relation of MMP 9 activity with LVEDD, FS, LVEF, and dp/dtmax ( r =0.92, -0.95, -0.96, -0.94, respectively, all P0.01). Conclusion MMP 2 and MMP 9 activities are associated with ventricular remo- deling- and heart function in a rat model of acute myocardial infarction. They may play an important role in promoting ventricular remodeling and cardiac dysfunction.