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目的:探讨黄嘌呤氧化酶(Xanthine oxidase,XO)抑制剂别嘌呤醇(Allopurinol)对心肌梗死(Myocardial infarction,MI)后大鼠心室重构和心功能的影响。方法:结扎冠脉前降支制作大鼠心肌梗死模型,随机分为假手术组(sham,n=5),心肌梗死组(MI,n=16)和别嘌呤醇组[50mg(/kg·d),n=15],28d后观察血流动力学和超声心动图的变化,并检测左心室重量指数(LVWI),心肌梗死面积,清除活性氧(Reactive oxygen species,ROS)活力,XO活力和蛋白表达。结果:与sham组比较,MI组LVWI,XO蛋白表达和活力升高,清除活性氧活力和心功能降低(P<0.01)。别嘌呤醇组与MI组比较,LVWI和XO活力降低,清除活性氧活力和心功能升高(P<0.05或P<0.01),但心率,动脉血压,梗死面积和XO蛋白表达在两组间差异无显著性(P>0.05)。结论:别嘌呤醇能够抑制心肌梗死后心室重构,改善心功能。其机制可能与抑制黄嘌呤氧化酶活性,减少活性氧的生成有关。
Objective: To investigate the effect of Allopurinol, an inhibitor of xanthine oxidase (XO), on ventricular remodeling and cardiac function in rats after myocardial infarction (MI). Methods: The model of myocardial infarction was established by ligating the anterior descending coronary artery in rats. The rats were randomly divided into sham operation group (n = 5), myocardial infarction group (MI, n = 16) and allopurinol group d), n = 15]. After 28 days, the changes of hemodynamics and echocardiography were observed. The left ventricular mass index (LVWI), myocardial infarct size, reactive oxygen species (ROS) And protein expression. Results: Compared with sham group, the expression of LVWI and XO protein in MI group increased and the activities of reactive oxygen species (ROS) and cardiac function were decreased (P <0.01). In allopurinol group, LVWI and XO activities were decreased, reactive oxygen species (ROS) and cardiac function were decreased (P <0.05 or P <0.01), but heart rate, arterial pressure, infarct size and XO protein expression were significantly decreased There was no significant difference (P> 0.05). Conclusion: Allopurinol can inhibit ventricular remodeling and improve cardiac function after myocardial infarction. The mechanism may be related to inhibition of xanthine oxidase activity, reduce the generation of reactive oxygen species.