Adamek Anna, Hu Kai, Bayer Barbara, Wagner Helga, Ertl Georg, Bauersachs Johann, Frantz Stefan
Medizinische Klinik und Poliklinik I der Universität Würzburg, Josef Schneider-Strasse 2, 97080 Würzburg, Germany.
Basic Res Cardiol. 2007 Jul;102(4):334-40. doi: 10.1007/s00395-007-0647-2. Epub 2007 Mar 8.
Proinflammatory proteins like inflammatory cytokines are implicated in myocardial depression and left ventricular remodeling after myocardial infarction. High-dose aspirin inhibits cytokine activation. Therefore, we tested the influence of high-dose aspirin treatment on left ventricular remodeling in mice after myocardial infarction.
Mice were treated for 4 weeks with placebo or aspirin (120 mg/kg per day) by Alzet mini-osmotic pumps after ligation of the left anterior descending coronary artery. Serial transthoracic echocardiography was performed at days 1, 7, and 28. Over the 4 weeks, mortality was not different between the groups (placebo 30.8%, aspirin 30.8%). On echocardiography, animals after myocardial infarction exhibited left ventricular dilatation (week 4, end-systolic area, placebo sham 8.9 +/- 1.7 vs. placebo MI 15.9 +/- 2.5 mm(2)), which was not changed by aspirin treatment (week 4, end-systolic area, aspirin MI 14.5 +/- 1.3 mm(2), p= ns vs. placebo MI). The expression of the proinflammatory cytokines TNF and IL-1beta were markedly upregulated in mice with myocardial infarction on placebo. Cytokine expression was significantly reduced by aspirin treatment while collagen deposition was not influenced.
Continuous aspirin treatment (120 mg/kg/d) reduces the expression of proinflammatory cytokines after myocardial infarction, but does not affect post-infarct cardiac remodeling and cardiac function.
促炎蛋白如炎性细胞因子与心肌梗死后的心肌抑制和左心室重构有关。高剂量阿司匹林可抑制细胞因子激活。因此,我们测试了高剂量阿司匹林治疗对心肌梗死后小鼠左心室重构的影响。
在结扎左冠状动脉前降支后,通过Alzet微型渗透泵对小鼠进行4周的安慰剂或阿司匹林(每天120mg/kg)治疗。在第1、7和28天进行系列经胸超声心动图检查。在4周内,两组的死亡率无差异(安慰剂组30.8%,阿司匹林组30.8%)。超声心动图显示,心肌梗死后的动物出现左心室扩张(第4周,收缩末期面积,安慰剂假手术组8.9±1.7 vs. 安慰剂心肌梗死组15.9±2.5mm²),阿司匹林治疗未改变这一情况(第4周,收缩末期面积,阿司匹林心肌梗死组14.5±1.3mm²,与安慰剂心肌梗死组相比p=无显著性差异)。安慰剂治疗的心肌梗死小鼠中促炎细胞因子TNF和IL-1β的表达明显上调。阿司匹林治疗可显著降低细胞因子表达,而胶原沉积不受影响。
持续阿司匹林治疗(120mg/kg/d)可降低心肌梗死后促炎细胞因子的表达,但不影响梗死后心脏重构和心脏功能。