Effects of Simvastatin on Sarcoplasmic Reticulum Calcium Adenosine Triphosphatase in Rabbits with Heart Failure
Jiang Wen-pin
Abstract
Jiang Wen-pin
Abstract
Objective To investigate the expression and function of sarcoplasmic reticulum calcium adenosine triphosphatase(SERCA2) in heart failure rabbit and the effects of simvastatin on the prevention of chronic heart failure.Methods Twenty-one rabbits were divided into three groups:sham operated group (n=7),heart failure group (n=7) and simvastatin group [n=7,10 mg/(kg· d)].Heart failure was induced by combination of volume and pressure overload.Seven weeks later,left ventricular shorten fraction (LVFS),left ventricular ejection fraction (LVEF),left ventricle end-systolic pressure (LVESP),left ventricle end-diastolic pressure (LVEDP) and left ventricular mass index (LVMI) were determined.Expression and function of SERCA2 were detected.Results Compared with the sham operated rabbits,LVMI [(3.61±0.09) vs (1.32±0.06)g/kg] and LVEDP were significantly increased LVFS,LVEF [(38.5±5.1)% vs (71.9±4.6)%] were decreased in heart failure rabbits (all P0.05).Simvastatin significantly decreased LVMI [(2.17±0.13)g/kg] and LVEDP,increased LVFS and LVEF [(62.2±3.3)%] (all P0.05),which was associated with increases in expression and function of SERCA2 [mRNA,heart failure group (0.70±0.04) vs sham operated group (1.06±0.16) vs simvastatin treated group (0.86±0.02),protein:heart failure group (0.69±0.04) vs sham operated group (1.02±0.02) vs simvastatin treated group (0.87±0.03),activity:heart failure group (8.32±0.15) vs sham operated group (15.01±1.00) vs simvastatin treated group (11.81±0.63) μmol Pi/(mg pro·h),all P0.05].Conclusion Simvastatin improved cardiac function,which was associated with upregulating expression and function of SERCA2.
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Objective To investigate the expression and function of sarcoplasmic reticulum calcium adenosine triphosphatase(SERCA2) in heart failure rabbit and the effects of simvastatin on the prevention of chronic heart failure.Methods Twenty-one rabbits were divided into three groups:sham operated group (n=7),heart failure group (n=7) and simvastatin group [n=7,10 mg/(kg· d)].Heart failure was induced by combination of volume and pressure overload.Seven weeks later,left ventricular shorten fraction (LVFS),left ventricular ejection fraction (LVEF),left ventricle end-systolic pressure (LVESP),left ventricle end-diastolic pressure (LVEDP) and left ventricular mass index (LVMI) were determined.Expression and function of SERCA2 were detected.Results Compared with the sham operated rabbits,LVMI [(3.61±0.09) vs (1.32±0.06)g/kg] and LVEDP were significantly increased LVFS,LVEF [(38.5±5.1)% vs (71.9±4.6)%] were decreased in heart failure rabbits (all P0.05).Simvastatin significantly decreased LVMI [(2.17±0.13)g/kg] and LVEDP,increased LVFS and LVEF [(62.2±3.3)%] (all P0.05),which was associated with increases in expression and function of SERCA2 [mRNA,heart failure group (0.70±0.04) vs sham operated group (1.06±0.16) vs simvastatin treated group (0.86±0.02),protein:heart failure group (0.69±0.04) vs sham operated group (1.02±0.02) vs simvastatin treated group (0.87±0.03),activity:heart failure group (8.32±0.15) vs sham operated group (15.01±1.00) vs simvastatin treated group (11.81±0.63) μmol Pi/(mg pro·h),all P0.05].Conclusion Simvastatin improved cardiac function,which was associated with upregulating expression and function of SERCA2.
Key concepts: Simvastatin, Preload, Internal medicine, Heart failure, Ventricle, Ejection fraction, Cardiology, Medicine