Effect of Hepatocyte Growth Factor on Mitral Regurgitation Caused by Acute Myocardial Infarction in Canines / 中国康复理论与实践

ABSTRACT

@#Objective To investigate the effect of hepatocyte growth factor (HGF) on mitral regurgitation caused by acute myocardial infarction in canines.Methods The acute myocardial infarction model was established by ligating proximal left anterior descending coronary artery (LAD) with 13 hybrid canines. The myocardial infarction model was successfuly established in 12 animals and those were randomly divided into the HGF-group and control group with 6 animals in each group. Canines of the HGF-group were injected with pc-DNA3-HGF 1 ml (about 300 μg) at the margin of infarcted myocardial and animals of the control group were injected with equal volume saline. The data were measured through echocardiography in the 1st, 4th and 8th week after ligation as following parameters left ventricular ejection fraction (LVEF), left ventricular end-systolic volume (LVESV), left atrial area, mitral regurgitation area and the ratio of left atrial area to mitral regurgitation area. Left ventricular myocardium specimens were obtained in the 8th week after ligation and stained with hematoxylin and eosin for histological examination or with picrosirius red staining to assess the collagen content.Results Compared with the control group, LVEF in the HGF-group increased in the 4th week after ligation; LVEF significantly improved and LVESV decreased in the 8th week after ligation ( P<0.05). In the 8th week after ligation, left atrial area, mitral regurgitation area and the ratio of left atrial area to mitral regurgitation area in the HGF-group were lower than that in the control group. In the HGF-group, neovascularization and fewer scars were observed histologically. Compared with the control group, the HGF-group showed higher capillary density in margin of infarcted area by factor Ⅷ-related immunohistochemistry staining ( P<0.01).Conclusion HGF gene can improve cardiac function and relieve mitral regurgitation after acute myocardial infarction by stimulating angiogenesis, reducing fibrosis, diminishing myocardiolysis and scarring.