Effect of Yuxingeng Fluid (愈心梗液) on Myocardial Energy Metabolism in Wistar Rats with Acute Myocardial Infarction

Objective: To examine the effect of Yuxingeng fluid (愈心梗液, YXGF) on myocardial energy metabolism in Wistar rats with acute myocardial infarction (AMI) by observing the ultrastructure of mitochondria and the enzyme activities of rat myocardial adenosine triphosphate (ATP), succinate dehydrogenase (SDH), acid phosphatase (ACP), alkaline phosphatase (ALP) and the content of glycogen. Methods; AMI models were established by ligature of left anterior descending coronary artery and then the rats with AMI were randomly divided into 7 groups: namely, blank group, model group, sham-operated group, captopil group, high-dose YXGF group, middle-dose YXGF group and low-dose YXGF group. From the next day after modeling, the rats were given YXGF through gastrogavage which lasted for 4 weeks. And then, the ultra-structure of mitochondria was observed by electronic microscope and the enzyme activities of ATP, SDH, ACP, ALP and the content of glycogen were determined. Results: Compared with model group, the other three groups of high-dose YXGF, middle-dose YXGF, low-dose YXGF and captopril group could protect the ultrastructure of mitochondria and significantly increase enzyme activities of ATP, SDH, ACP, ALP and the content of glycogen (P<0.01). Conclusion: YXGF can protect mitochondria and increase myocardial enzyme activities and the content of glycogen, which may be one of the mechanisms intervening in the pathological course of the early ventricular remodeling in rats with AMI.

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

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。

愈心梗液防治大鼠急性心肌梗死后心室重构的机理研究

目的:通过观察心肌组织和血浆内皮素(ET)、血管紧张素Ⅱ(Ang Ⅱ)含量的变化,研究愈心梗液防治急性心肌梗死(AMI)后心室重构的机理。方法:结扎 Wistar 大鼠冠状动脉左前降支,体表心电图Ⅱ导示 ST-T 弓背抬高,证实 AMI 形成后,将大鼠随机分为6组,于手术后第2天开始灌胃给药,连续4周。然后处死大鼠,观察各组大鼠心脏指数、心室重量和心肌组织及血中 ET、Ang Ⅱ含量。结果:与模型组比较,愈心梗液大、中剂量和开博通皆可显著降低 AMI 大鼠心脏指数(P<0.01)和左室重量,愈心梗液大剂量和开搏通可显著降低心肌组织及血浆中 ET、AngⅡ含量(P<0.01和P<0.05)。愈心梗液中、小剂量亦能明显降低心肌组织中 ET 的含量(P<0.05)。结论:愈心梗液可显著降低 AMI 大鼠左室重量和心脏指数,其降低心肌组织及血浆中 ET 和 AngⅡ的含量可能是防治 AMI 后期心室重构的作用机理之一。