首页> 外文期刊>Basic Research in Cardiology: Official Journal of the German Association of Cardiovascular Research >High dose aspirin and left ventricular remodeling after myocardial infarction: aspirin and myocardial infarction.
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High dose aspirin and left ventricular remodeling after myocardial infarction: aspirin and myocardial infarction.

机译:心肌梗死后大剂量阿司匹林和左心室重构:阿司匹林和心肌梗塞。

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BACKGROUND: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.
机译:背景:诸如炎症性细胞因子之类的促炎蛋白与心肌梗塞后的心肌抑制和左心室重构有关。大剂量阿司匹林抑制细胞因子的激活。因此,我们测试了大剂量阿司匹林治疗对心肌梗塞后小鼠左心室重构的影响。方法和结果:结扎左冠状动脉前降支后,通过Alzet微型渗透泵用安慰剂或阿司匹林(每天120 mg / kg)治疗小鼠4周。在第1、7和28天进行连续经胸超声心动图检查。在4周内,两组间的死亡率无差异(安慰剂为30.8%,阿司匹林为30.8%)。在超声心动图上,心肌梗死后的动物表现出左心室扩张(第4周,收缩末期区域,安慰剂假手术8.9 +/- 1.7 vs.安慰剂MI 15.9 +/- 2.5 mm(2)),阿司匹林治疗并没有改变(第4周,收缩末期面积,阿司匹林MI 14.5 +/- 1.3 mm(2),相对于安慰剂MI,p = ns。在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。阿司匹林治疗可显着降低细胞因子的表达,而胶原蛋白的沉积不受影响。结论:阿司匹林持续治疗(120 mg / 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塑和心脏功能。

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