愈心梗液保护急性心肌梗死后心力衰竭大鼠心肌细胞和线粒体超微结构及抗氧化作用的实验研究

Study of Yuxingeng Fluid on Protection of Ultrastructure of Myocardial Cell,Mitochondria and Antioxidation in Wistar Rats with Heart Failure After Acute Myocardial Infarction

目的观察愈心梗液保护大鼠急性心肌梗死(AM I)后心力衰竭心肌细胞及线粒体超微结构和抗氧化的作用。方法结扎W istar大鼠冠状动脉造成实验性AM I心力衰竭模型,并使之长期存活。造模成功后,大鼠随机分为7组,每组10只,即空白组、假手术(只穿刺不结扎)组、模型组、开搏通组、愈心梗液大、中、小剂量组。各给药组于手术即日起开始灌胃给药,连续4周。4周后麻醉处死大鼠,心脏组织切片处理后通过电镜和光镜观察心肌细胞及线粒体的形态结构及测定心肌细胞的横截面积、周长,同时测定大鼠心肌组织和血清中丙二醛(MDA)和超氧化物歧化酶(SOD)的含量。结果动物造模4周后,大鼠心肌细胞中心肌纤维排列杂乱,图像系统测量显示心肌细胞横截面积增大、周长增加。与模型组比较,愈心梗液大、中剂量可显著降低大鼠心肌细胞横截面积、周长和直径(和模型比较,P<0.01),减少大鼠心肌组织和血清中MDA的含量和升高SOD的含量。结论愈心梗液可抑制大鼠AM I后心肌细胞的代偿性增大,保护线粒体结构的相对完整性,提高大鼠的抗氧化能力,干预AM I大鼠心室重构VR的病理过程,有改善AM I后心力衰竭的作用。

Objective To observe the effect of Yuxingeng fluid （YXGF） on uhrastructure of mitochondria, myocardial cell and antioxidation in Wistar rats with heart failure after acute myocardial infarction （AMI）. Methods AMI models were established by ligaturing left anterior descending coronary artery, and rats with AMI were randomly divided into 7 groups. From the next day after modeling, the rats were administered with YXGF through the stomach tube and lasting for 4 weeks. Then, the uhrastructure of mitochondria and myocardial cell was observed by electronic microscope and the enzyme activities of malonaldehyde and erythrocuprein were measured. Results Comparing with model group, high - dose YXGF, middle - dose YX- GF and captopril protected the uhrastructure of mitochondria and myocardiaol cell, significantly increased enzyme activities of SOD and deceased MDA （P 〈 0.01）. Conclusion YXGF could protect mitochondria and myocardial cell and had a beneficial effect on antioxidation, which may be one of the mechanisms intervening the pathological course of the early ventricular remodeling （VR） in rats with AMI.