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Evaluation of effect of atorvastatin on left ventricular systolic function in rats with myocardial infarction via 2D-STI technique

机译:2D-STI技术评价阿托伐他汀对心肌梗死大鼠左室收缩功能的影响

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摘要

This report aims to evaluate the effect of atorvastatin (Ator) on left ventricular systolic function in myocardial infarction (MI) rats. Forty healthy adult Sprague-Dawley rats were randomly divided into four groups: Ator group, MI group, sham-operation group and normal group. The left anterior descending coronary arteries were ligated to establish the MI model; after modeling, the Ator group was treated with Ator for 4 consecutive weeks. The echocardiographic detection was performed; the left ventricular myocardial systolic peak velocities, strain and strain rates were analyzed using the 2D-STI technique. After 4 weeks, myocardial tissues were taken from all rats and received the pathological examination. Left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) in Ator group and MI group were increased after operation, but left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were decreased; myocardial function were decreased significantly (p<0.05). After Ator treatment, myocardial function at the 3rd and 4th week after operation increased significantly (p<0.05). After Ator treatment, LVEDD and LVESD decreased while LVEF and LVFS increased in Ator group at the 3rd and 4th week after operation compared with MI group (p<0.05). At the 4th week after operation, LVEDD and LVESD in Ator group were decreased compared with those at the 1st and 2nd week after operation, but LVEF and LVFS were increased compared with those at the 1st, 2nd and 3rd week after operation (p<0.05). Pathological examination showed that necrosis and fibrosis of myocardial cells and inflammatory reaction were obvious in MI group. The inflammatory reaction of myocardial cells and myocardial fibrosis were lighter in Ator group. Ator can effectively improve the left ventricular systolic function in MI rats, which could be related to the reduction of response to inflammation and fibrosis.
机译:本报告旨在评估阿托伐他汀(Ator)对心肌梗死(MI)大鼠左心室收缩功能的影响。 40只健康成年Sprague-Dawley大鼠随机分为四组:阿托尔组,心梗组,假手术组和正常组。结扎左冠状动脉前降支以建立MI模型。建模后,将Ator组连续4周接受Ator治疗。进行超声心动图检测;使用2D-STI技术分析左心室心肌收缩峰值速度,应变和应变率。 4周后,从所有大鼠中取出心肌组织并进行病理检查。 Ator组和MI组术后左室舒张末期直径(LVEDD)和左室收缩末期直径(LVESD)增加,但左室射血分数(LVEF)和左室分数缩短(LVFS)降低;心肌功能明显下降(p <0.05)。 Ator治疗后,术后第3和第4周的心肌功能显着提高(p <0.05)。与MI组相比,Ator组在术后第3周和第4周接受Ator治疗后,LVEDD和LVESD降低,而LVEF和LVFS升高(p <0.05)。术后第4周,Ator组的LVEDD和LVESD较术后第1、2周有所下降,但LVEF和LVFS较术后第1、2、3周有所升高(p <0.05)。 )。病理检查发现MI组心肌细胞坏死,纤维化及炎症反应明显。 Ator组心肌细胞的炎症反应和心肌纤维化较轻。 Ator可以有效改善MI大鼠的左心室收缩功能,这可能与对炎症和纤维化的反应减少有关。

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