摘要
目的观察实验性急性心肌梗死(AMI)后大鼠心脏结构的变化和动物血浆、心肌组织的内皮素(ET)、血管紧张素Ⅱ(AngⅡ)的水平,探讨复方芪丹液防治AMI后心室重构(VR)的作用机制。方法结扎大鼠冠状动脉左前降支,造成动物实验性AMI模型,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,于术后第2日开始灌胃给药,连续4周。麻醉处死大鼠,观察各组大鼠心脏指数、心室重量、心肌细胞大小等心脏结构和血浆及心肌组织中ET、AngⅡ的含量。结果服用复方芪丹液4周后,与模型组比较,中药大、中剂量和开博通皆可明显降低AMI大鼠心脏指数(P<0.01)和左室重量;对血浆和心肌组织中ET、AngⅡ含量亦较模型组明显降低(P<0.01和P<0.05),并可减少左室心肌细胞的面积、周长和直径。结论复方芪丹液可显著降低AMI大鼠左室重量、心脏指数,抑制大鼠左室心肌细胞的增大,降低大鼠血浆及心肌组织中ET和AngⅡ的含量。抑制大鼠血浆和心肌组织的血管活性物质可能是防治AMI后早期VR的作用机制之一。
Objective To examine the acting mechanism of Qidan complex fluid(QDF) on early ventricular remodeling in wistar rats with acute myocardial infarction(AMI) by measuring the cardiac index(CI),left ventricular weight(LVW) and cardiac myocyte dimension and observing the concentration of endothelin(ET) and angiotensin Ⅱ(AngⅡ) in the plasma and myocardium. Methods AMI models were established by ligaturing left anterior descending coronary artery and the rats with AMI were randomly divided into 6 groups: namely, model group, sham-operated group, captopril group, high-dose QDF group, middle-dose QDF group and low-dose group. From the next day after modeling, the rats were given QDF through the stomach tube and lasted for 4 weeks. And then, CI, LVW and concentration of ET and AngⅡ in the plasma and myocardium were tested. Results Comparing with model control group, high-dose QDF, middle-dose QDF and captopril can significantly decrease CI, LVW, cardiac cell dimension and content of ET and AngⅡ in both plasma and myocardium (P<0.05 and P<0.01=. Conclusion QDF can remarkably reduce the LVW, CI and concentration of ET and AngⅡ, lowering concentration of ET and AngⅡmay be one of mechanisms intervening the pathological course of the early ventricular remodeling in rats with AMI.
出处
《中国心血管病研究》
CAS
2005年第4期301-304,共4页
Chinese Journal of Cardiovascular Research
基金
国家自然科学基金课题资助项目(批准号:39870942)
