余志利, 杨波, 初洪钢, 陈江斌, 陈绪江, 姚维. 缬沙坦对急性心肌梗死大鼠左室重构及心功能的影响[J]. 心脏杂志, 2009, 21(2): 193-196.
    引用本文: 余志利, 杨波, 初洪钢, 陈江斌, 陈绪江, 姚维. 缬沙坦对急性心肌梗死大鼠左室重构及心功能的影响[J]. 心脏杂志, 2009, 21(2): 193-196.
    Influence of valsartan on left ventricular remodeling and heart function in rats with acute myocardial infarction[J]. Chinese Heart Journal, 2009, 21(2): 193-196.
    Citation: Influence of valsartan on left ventricular remodeling and heart function in rats with acute myocardial infarction[J]. Chinese Heart Journal, 2009, 21(2): 193-196.

    缬沙坦对急性心肌梗死大鼠左室重构及心功能的影响

    Influence of valsartan on left ventricular remodeling and heart function in rats with acute myocardial infarction

    • 摘要: 目的 研究缬沙坦对大鼠急性心肌梗死(AMI)后左室重构及心功能的影响。方法 将80只雌性SD大鼠AMI后6 h随机分为:梗死对照组(MI-C组,n=30)、缬沙坦治疗组(MI-V组,n=30)及假手术组(Sham组,n=20)。MI-C组及MI-V组结扎冠状动脉左室支建立AMI模型,Sham组只在相同部位穿线后不结扎。MI-V组:将缬沙坦20 mg/(kg·d)以生理盐水15 ml/kg溶解后灌胃,每日2次,共7 d;MI-V组和Sham组:均以等量生理盐水灌胃,每日2次,共7 d。分别于AMI后12 h、3 d 及7 d,测定血流动力学,进行超声和形态学检查。结果 与Sham组比较,MI-C组的左室收缩压(LVSP)、左室内压最大上升速率(+dp/dt)和左室内压最大下降速率(-dp/dt)显著降低(分别为P<0.05及P<0.01);左室舒张末压(LVEDP)显著增加(P<0.01);左室舒张末期容积(LVEDV)、短轴(D)、左室相对质量(LVWI)逐渐增加,至7 d时显著增加(P<0.05或P<0.01);长轴(L)、球形指数、短轴缩短率(FS)逐渐降低,至7 d时显著降低(P<0.05或P<0.01)。与MI-C组比较,MI-V组的LVSP、+dp/dt、-dp/dt显著回升(P<0.05或P<0.01),LVEDP显著下降(P<0.05或P<0.01),LVWI逐渐下降,至7 d时降低显著(P<0.05),梗死范围从3 d、7 d开始显著减小(P<0.05)。LVEDV、D、LVWI及梗死范围均下降,至7 d时显著降低(P<0.05或P<0.01),L、球形指数、FS逐渐升高,至7 d时显著上升(P<0.05或P<0.01)。结论 缬沙坦能减轻心肌梗死后左室构型的改变,改善早期AMI后大鼠的心功能,抑制左室重构,改善左室的功能。

       

      Abstract: AIM To investigate the effect of valsartan on the left ventricular remodeling and heart function in rats with acute myocardial infarction (AMI). METHODS Six hours after ligating left coronary artery, 80 female Sprague Dawley rats were divided randomly into Sham operation group (Sham group, n=20), MI control group (MI-C group, n=30) and MI valsartan group (MI-V group, n=30). MI-C group and MI-V group undergone acute myocardial infarction by ligation of left anterior descending coronary artery. Sham group were treated in the same way as previously described except for coronary ligation. In MI-V group, valsartan was orally administered 20 mg/(kg·d), twice a day and this procedure lasted 7 days. In Sham group and MI-C group, only 4 g/L saline was orally administered. After 12 hours, 3 days and 7 days of therapy, we analyzed the echocardiography parameters and structure parameters. RESULTS Compared with those in Sham group, left ventricular systolic pressure, left ventricular +dp/dtmax and -dp/dtmax markedly decreased(P<0.05), while left ventricular end diastolic pressure markedly increased(P<0.05) and left ventricular weight index markedly increased(P<0.05) in 7 days in MI-C group. Left ventricular end diastolic volume, short axes and left ventricular weight index markedly decreased(P<0.05 or 0.01) in 7 days. Long axes, Sphericity index and fractional shortening markedly decreased(P<0.05 or 0.01) in 7 days in MI-C group. Compared with those in MI-C group, LVSP, +dp/dt, -dp/dt and LVEDP markedly increased(P<0.05)while LVWI markedly decreased(P<0.05) in 7 days in MI-V group. Infarction regional markedlyalso decreased(P<0.05) in 3 days and 7 days in MI-V group. LVEDV, D and LVWI markedly decreased(P<0.05 or 0.01) in 7 days. L, sphericity index and FS markedly increased(P<0.05 or 0.01) in 7 days in MI-V group. CONCLUSION Valsartan restrains left ventricular remodeling and improves heart function after AMI.

       

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