Effect of simvastatin on angiogenesis of ischemic myocardium with acute myocardial infarcted in rats

Objective To investigate whether simvastatin can mobilize stem cells to the infracted myocardium with acute myocardial infarted (AMI) and promote angiogenesis of ischemic myocardium in rat.Meth- ods Sixty rats were randomly assigned to test group,control group and sham operation group.The AMI model was created with the left coronary artery (LCA) ligated in rats.Simvastatin (50 mg·kg·d~(-1)) was admin- istered with gastric gavage in test group.After 2 and 4 weeks of interven- tion,echocardiography and hemodynamic studies were performed.The wet-to-dry ratio of lungs was measured in all rats.The left ventricle of rat were fixed and analyzed.The positive of CD34 cells in peripheral blood and infarcted myocardium,the capillary density in myocardium and the expression of vascular endothelial growth factor (VEGF) in all groups were evaluated with immunohistochemistrical staining.Results The left ventricular systolic pressure (LVSP),maximum rate of left ventricular pressure rise (+dp/dt_(max)),maximum rate of left ventricular pressure de- cay (-dp/dt_(max)) and left ventricular eject factor (LVEF) in test group were higher than those in control group(P0.05).The left ventricular end diastolic pressure (LVEDP) and the wet-to-dry ratio of the lungs were lower than that in control group(P0.05).The positive of CD34 cells,the capillary density and the A of VEGF in the infarcted myocardi- um of test group were significantly higher than those in control group (P 0.05).Conclusion Simvastatin can both mobilize the endothelial stem cells to home and promote capillary formation in the infarcted myocardium.Simvastatin may upregulate the VEGF protein expression then increase angiogenesis in infarcted myocardium and improve heart function.