Enomoto S, Yoshiyama M, Omura T, Matsumoto R, Kusuyama T, Kim S, Izumi Y, Akioka K, Iwao H, Takeuchi K, Yoshikawa J
Department of Internal Medicine and Cardiology, Osaka City University Medical School, Japan.
Heart. 2005 Dec;91(12):1595-600. doi: 10.1136/hrt.2004.046540. Epub 2005 Mar 29.
To examine the effects of eplerenone, a selective aldosterone blocker, on cardiac function after myocardial infarction (MI) and myocardial remodelling related transcriptional factors and mRNA expression in non-infarcted myocardium.
MI was induced by ligation of the coronary artery in Wistar rats. Rats were randomly assigned to a vehicle treated group or an eplerenone treated group (100 mg/kg/day).
At four weeks after MI, left ventricular (LV) end diastolic pressure, LV weight, and LV end diastolic dimension were increased in MI rats. Eplerenone significantly reduced the increase in LV end diastolic pressure, LV weight, and LV end diastolic dimension. In the MI rats the decreased ejection fraction indicated systolic dysfunction and the increased E wave to A wave ratio and E deceleration rate indicated diastolic dysfunction. Eplerenone significantly attenuated this systolic and diastolic dysfunction. Myocardial interstitial fibrosis, transcriptional activities of activator protein 1 and nuclear factor kappaB, and mRNA expression of monocyte chemoattractant protein 1, plasminogen activator inhibitor 1, atrial natriuretic peptide, brain natriuretic peptide, and collagen types I and III were significantly increased at four weeks after MI. Eplerenone significantly attenuated interstitial fibrosis and suppressed transcriptional activity and mRNA expression of these genes.
When administered after MI, eplerenone prevents cardiac remodelling accompanied by systolic and diastolic dysfunction and inhibits abnormal myocardial transcriptional activities and gene expression.
研究选择性醛固酮阻滞剂依普利酮对心肌梗死后心脏功能以及非梗死心肌中与心肌重塑相关转录因子和mRNA表达的影响。
通过结扎Wistar大鼠冠状动脉诱导心肌梗死。大鼠被随机分为溶剂处理组或依普利酮处理组(100毫克/千克/天)。
心肌梗死后四周,心肌梗死大鼠的左心室舒张末期压力、左心室重量和左心室舒张末期内径增加。依普利酮显著降低了左心室舒张末期压力、左心室重量和左心室舒张末期内径的增加。在心肌梗死大鼠中,射血分数降低表明收缩功能障碍,E波与A波比值增加和E波减速速率增加表明舒张功能障碍。依普利酮显著减轻了这种收缩和舒张功能障碍。心肌梗死后四周,心肌间质纤维化、活化蛋白1和核因子κB的转录活性以及单核细胞趋化蛋白1、纤溶酶原激活物抑制剂1、心房利钠肽、脑利钠肽以及I型和III型胶原的mRNA表达显著增加。依普利酮显著减轻间质纤维化并抑制这些基因的转录活性和mRNA表达。
心肌梗死后给予依普利酮可预防伴有收缩和舒张功能障碍的心脏重塑,并抑制异常的心肌转录活性和基因表达。