曲美他嗪对心梗后心衰大鼠心功能及心肌超微结构的影响  

Effects of Trimetazidine on the Cardiac Function and Ultrastructure in Rats with Heart Failure after Myocardial Infarction

作　　者：石洁[1] 阿不都吉力力阿不力孜 商秀洋[1] 胡元会[1] 

机构地区：[1]中国中医科学院广安门医院,北京100053

出　　处：《中西医结合心脑血管病杂志》2017年第24期3114-3118,共5页Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease

基　　金：博士后基金(201104224)

摘　　要：目的研究曲美他嗪对心肌梗死后心衰大鼠心功能及心肌超微结构的影响。方法采用结扎SD大鼠前降支复制心肌梗死后心衰模型,以曲美他嗪于造模后72h灌胃给药,以只穿线不结扎前降支为假手术组。造模后及给药8周后分别行心脏超声检查,并于给药第8周,于末次给药后12h后采集心肌样本,行HE染色和Masson染色。结果治疗后与模型组比较,曲美他嗪组左室舒张末内径(LVIDd)和左室收缩末内径(LVIDs)均减低,有统计学意义(P<0.05和<0.01);左室射血分数(LVEF)、左室短轴缩短率(FS)、心输出量(CO)均明显增加,有统计学意义<0.01)。曲美他嗪组治疗后与治疗前比较,治疗后LVIDd与治疗前无明显变化;治疗后LVIDs较治疗前减低(P<0.05);治疗后EF、FS较治疗前明显增加(P<0.01);治疗后CO较治疗前增加(P<0.05)。光镜下观察心肌细胞,模型组心肌梗死灶范围广泛,内坏死组织及炎性细胞浸润,心肌纤维排列紊乱,梗死灶内有散在岛状分布的存活心肌细胞,坏死心肌细胞被胶原组织代替。曲美他嗪组心肌梗死灶较局限,心肌细胞部分坏死,散在心肌纤维断裂消失,可见梗死灶内呈岛状分布的存活心肌细胞,可见成纤维细胞和肉芽组织增生较模型组增多,部分心肌细胞被胶原纤维代替。结论曲美他嗪能有效改善心梗后心衰大鼠的收缩功能,并改善其心肌超微结构,抑制细胞外基质胶原纤维的增生。Objective To study the effect of trimetazidine on cardiac function and ultrastructure in heart failure rats after myocardial infarction.Methods Ligation of left anterior descending coronary artery was performed in myocardial infarction-induced heart failure models in rats.Rats were randomly divided into sham group,model group and trimetadizine group after the success of building.Echcardiography was used to observe cardiac function changes of rats.Hematoxylin-Eosin（HE）staining and Masson staining were used to observe histopathologic changes of myocardial tissue under light microscope.Results Compared with the rats in model group,left ventricular internal diameter at diastole（LVIDd）and systole（LVIDs）in trimetadizine group were significantly reduced after 8 weeks＇ drug therapy.The ejection fraction（LVEF）,fractional shortening（FS）and cardiac output（CO）in trimetadizine group were increased obviously.Under light microscope,HE staining showed that there was wide range of myocardial infarction and disordered arrangement of myocardial fibers in model group cells.A lot of collagen fibre tissues were seen,while granulation tissue rared.In trimetadizine group,there was limited myocardial infarctions area.Myocardial fiber arrangement was irregular.Fibroblast and granylation tissue hyperplasia increased more than model group.Masson staining showed that myocardial cell were hypertrophied,arranged disorderly,and some were supplemented by collagen tissues in model group.The partial myocardial cells were replaced by collagen fibers and collagen fibers were mingled with myocardial cells in trimetadizine group.Conclusion Trimetazidine can effectively improve the contractile function of heart failure rats after myocardial infarction,and improve myocardial ultrastructure and inhibit the proliferation of extracellular matrix collagen fibers.

关 键 词：心梗后心衰 曲美他嗪 大鼠 心功能 超微结构 

分 类 号：R542.22[医药卫生—心血管疾病]