【摘要】 目的　评价醛固酮受体拮抗剂安体舒通和血管紧张素Ⅱ受体拮抗剂替米沙坦对心肌梗死 (AMI)不伴有心功能异常大鼠的作用和相关激素表达的影响。方法　SD大鼠心肌梗死模型建立 2 4h后 ,随机分为 4组 :AMI组、替米沙坦组 (10mg·kg-1·d-1)、安体舒通组 (2 0mg·kg-1·d-1)和合用组 ,并以假手术组为对照。 6w后 ,心脏超声、血流动力学、形态学检测心功能和心室重塑过程 ,并检测血浆、心肌血管紧张素Ⅱ、醛固酮和TNF -α水平。结果　各组心肌梗死面积差异没有显著性 (P >0 0 5 ) ,替米沙坦组和合用组显著降低LVEDP并增加了LVESP ,安体舒通组仅仅减少了LVEDP ,各组CVF表达均显著下降 (P <0 0 5 ,0 0 1) ,合用组没有进一步的下降。AMI组心肌醛固酮和AngⅡ表达分别增加 3 3和 2 1倍 ,替米沙坦组和合用组表达显著下降 ,(P <0 0 5 ,0 0 1)。结论　AMI后组织特异性的激活RAS系统 ,替米沙坦干预可以改善心室重塑 ,抑制心肌RAS的表达 ,与安体舒通合用没有协同作用。更多还原

【Abstract】 Objectives To evaluate the effect of mineralocorticoid receptor antagonist(MRA) spironolactone and angiotensin Ⅱ receptor blockade(ARB) telmisartan on post-infarct left ventricular without ventricular dysfunction and the role of the cardiac steroidogenic system. Methods 24h after left anterior coronary artery ligations, rats were randomly divided into untreated myocardial infarction (MI) group or spironolactone (20 mg·kg -1·d -1), telmisartan (20 mg·kg -1·d -1), spironolactone plus telmisartan treated MI groups for 6 weeks. Sham-operated rats were served as controls. The ventricular remodeling procedure and the expression of ang II, aldosterone and TNF-a were examined. Results The infracted area of all groups showed no difference (P>0.05). The level of LVEDP were decreased and LVESP increased in telmisartan and combined group (P<0.05,0.01); in the spironolactone group, only LVEDP decreased (P<0.05); the level of CVF decreased in all groups(P<0.05,0.01); In the non-infarcted myocardium of the left ventricle(LV) of AMI group, the level of aldosterone was raised by 3.3-times, also induced a 2.1-time increase of cardiac ang Ⅱ level. Such cardiac regulations were completely prevented by treatment of telmisartan. Conclusions AMI associates with tissue-specific activation of myocardial RAS, spironolactone combined with telmisartan can influence infarcted LV remodeling, but no better than telmisartan alone in association with the suppression of the activation of RAS in MI rats without ventricular dysfunction.更多还原