缬沙坦对家兔梗死心肌MDA、SOD、ATPase活性的影响

Effect of Valsartan on the MDA,SOD,ATPase activity of myocardial infarction in rabbit

目的:探讨缬沙坦(Valsartan,VAL)对心肌梗死(MI)作用及其作用机制。方法:结扎冠状动脉左前降支建立心肌梗死建模,随即分为假手术组、心肌梗死组、VAL组。然后分别在各组中应用BL-420F生物机能实验系统测定右颈总动脉插入动脉导管的心肌梗死(MI)的左室收缩压(LVSP)、左室舒张末压(LVEDP);分别采用黄嘌呤氧化法和硫代巴比妥酸显色法测定心肌丙二醛(MDA)和超氧化物歧化酶(SOD)含量以及应用定磷法心肌细胞细胞膜Na+-K+-ATPase、Ca2+-ATPase活性。结果:VAL可降低MI家兔的收缩压不明显(P>0.05),但降低舒张末降低明显(P<0.01);VAL使MI家兔增高的MAD显著降低(P<0.01);使MI家兔降低的SOD值显著恢复、增加(P<0.01);VAL可使MI家兔降低的Na+-K+-ATPase和Ca2+-ATPase活性恢复、增加(P<0.05)。结论:VAL可能通过稳定细胞膜抗脂质过氧化反应及提高清除氧自由基以及促进MI后心肌细胞膜Na+-K+-ATPase ATPase和Ca2+-AT-Pase活性的途径改善心肌梗死(MI)作用。

Objectives： To investigate the effects of Valsartan on myocardial infarction （MI） and its mechanism. Method： The model of MI was established by ligating coronary artery left falling branch firstly. Then sham-operation group, MI group, Valsartan group were divided into. After inserting right arteria carotis communis anterior with ducts, left volume systolic pressure （LVSP）, left volume diastole end pressure （LVEDP） were measured to each group by using BL-420F biology function experiment system separately, and by using Xanthine oxidation and 2-Thiobarbituric acid Color development process separately; Cardiac muscle Malondialdehyde （MDA） and Superoxide dismutase （SOD） content were determined as well as myocardial cell membrane Na^＋-K^＋-ATPase, the Ca^2＋-ATPase activity were detected by using quantitative analysis of phosphorus. Result： Valsartan decreased rabbit MI systolic pressure not significantly （P〉0.05）, hoever, decreased diastole pressure significantly （P〈0.01）; Valsartan restored MDA of MI to normal level which it ever was decreased in advance when model was established （P〈0.01）; Valsartan restored SOD of MI near to normal level which it ever was increased in advance when model was established （P〈0.01）; Valsartan could increased and restored Na^＋-K^＋-ATPase and Ca^2＋-ATPase enzyme activity which it ever was increased in advance when model was established. （P〈0.05）. Conclusion： Valsartan improved MI function possibly by the way of enhancing the elimination of oxygen free radical and stabilizing cell membrane to anti-lipid peroxidization as well as promoting Na^＋-K^＋-ATPase ATPase and Ca^2＋-ATPase activity of myocardial cell after MI.