| Abstract
| - Abstract. Objective: The purpose of this study was to examine the effect of amlodipine, a long-acting calcium antagonist, on the left ventricular remodeling, including systolic and diastolic dysfunction, the change of cardiac gene expression in the myocardial infarcted rats (MI). Methods: On the first day after myocardial infarction, the animals were randomly assigned to amlodipine treatment (n=8) or untreated groups (MI; n=9). We then performed Doppler-echocardiographic examinations and measured the hemodynamics at four weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. Results: Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 22±1 mmHg and 5±1 mmHg. Amlodipine reduced LVEDP and CVP to 15±1 mmHg (P<0.01) and 3±0 mmHg (P<0.01). The weight of right ventricle in MI was significantly larger than in the control rats (Control; 0.48±0.01 g/kg, MI; 0.79±0.04 g/kg, P<0.01). Left ventricular end-diastolic dimension (LVDd) in MI increased to 10.3±0.3 mm (P<0.01) (Control; 6.2±0.3 mm). Amlodipine prevented an increase of the weight of right ventricle (0.62±0.03 g/kg, P<0.01) and LVDd (7.9±0.2 mm, P<0.01 to MI). The rats in MI showed systolic dysfunction shown by the decreased fractional shortening (Control; 31±2% versus MI; 15±1%, P<0.01), and diastolic dysfunction shown by E wave deceleration rate (Control; 18.1±2.0 m/s2, MI; 32.6±2.1 m/s2, P<0.01). Amlodipine significantly prevented systolic and diastolic dysfunction. The increases in β-MHC, α-skeletal actin, and ANP mRNAs in the non-infarcted left ventricle and right ventricle at four weeks after the myocardial infarction were all significantly suppressed by the treatment with amlodipine. On the other hand, depressed α-MHC was restored to normal levels by amlodipine in both regions. Conclusions: Amlodipine prevents the left ventricular remodeling process accompanied by systolic and diastolic dysfunction, and inhibits abnormal cardiac gene expression after myocardial infarction.
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