Effects of pravastatin on ventricular remodeling and heart function after myocardial infarction in rats.
GU Shui-ming
Abstract
GU Shui-ming
Abstract
Objective To evaluate the effects of pravastatin on ventricular remodeling after acute myocardial infarction(AMI) in rats. Methods AMI was established by ligation of the anterior descending coronary artery in male SD rats. Twenty-four hours after the procedure, the 24 surviving rats were grouped randomly as AMI control(n=12)and pravastatin treatment(20 mg.kg~(-1).d~(-1), n=12). Sham-operated group(n=8) was taken randomly as non-infarction control. Six weeks after treatment with the drug and placebo by gastric gavage, the heart function and left ventricular remodeling were assessed by echocardiography and hemodynamic measurements. Ventricular weight (VW)/body weight(BW) ratio was determinated. The expressions of myocardial collagen type I and I/III collagen ratio were detected by immunohistochemistry. Results Compared with sham-operated group, left ventricular end-diastolic pressure〔LVEDP,(25.00±2.52)、(3.71±1.95)mm Hg〕, left ventricular end-diastolic diameter〔LVEDD,(0.61±0.04)、(0.39±0.01)mm〕, LVW/BW, RVW/ BW, expressions of collagen I , and I/III collagen ratio were all increased significantly (P0.01);whereas the maximal rate of rise and fall (dp/dtmax and dp/dtmin)of left ventricular pressure, fractional shortening(FS) and ejection fraction(EF)were all decreased significantly in MI group (P0.01). In comparison with AMI group, LVEDP, LVEDD, LVW/BW, RVW/BW, collagen I, and I/III collagen ratio were all decreased significantly (P0.05 or 0.01); while dp/dtmax, dp/dtmin, LVEF, and FS were all increased significantly in pravastatin treatment group (P0.05 or 0.01). Conclusions Pravastatin can prevent left ventricular remodeling after AMI in rats and improve cardiac function. Statins may have therapeutic benefits in patients with heart failure.
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Objective To evaluate the effects of pravastatin on ventricular remodeling after acute myocardial infarction(AMI) in rats. Methods AMI was established by ligation of the anterior descending coronary artery in male SD rats. Twenty-four hours after the procedure, the 24 surviving rats were grouped randomly as AMI control(n=12)and pravastatin treatment(20 mg.kg~(-1).d~(-1), n=12). Sham-operated group(n=8) was taken randomly as non-infarction control. Six weeks after treatment with the drug and placebo by gastric gavage, the heart function and left ventricular remodeling were assessed by echocardiography and hemodynamic measurements. Ventricular weight (VW)/body weight(BW) ratio was determinated. The expressions of myocardial collagen type I and I/III collagen ratio were detected by immunohistochemistry. Results Compared with sham-operated group, left ventricular end-diastolic pressure〔LVEDP,(25.00±2.52)、(3.71±1.95)mm Hg〕, left ventricular end-diastolic diameter〔LVEDD,(0.61±0.04)、(0.39±0.01)mm〕, LVW/BW, RVW/ BW, expressions of collagen I , and I/III collagen ratio were all increased significantly (P0.01);whereas the maximal rate of rise and fall (dp/dtmax and dp/dtmin)of left ventricular pressure, fractional shortening(FS) and ejection fraction(EF)were all decreased significantly in MI group (P0.01). In comparison with AMI group, LVEDP, LVEDD, LVW/BW, RVW/BW, collagen I, and I/III collagen ratio were all decreased significantly (P0.05 or 0.01); while dp/dtmax, dp/dtmin, LVEF, and FS were all increased significantly in pravastatin treatment group (P0.05 or 0.01). Conclusions Pravastatin can prevent left ventricular remodeling after AMI in rats and improve cardiac function. Statins may have therapeutic benefits in patients with heart failure.
Key concepts: Preload, Myocardial infarction, Medicine, Ejection fraction, Internal medicine, Cardiology, Ventricular remodeling, Cardiac function curve