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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。
Objective: To investigate the effect of valsartan (VAL) on myocardial infarction (MI) and its mechanism. Methods: The model of myocardial infarction was established by ligation of the left anterior descending coronary artery and then divided into sham operation group, myocardial infarction group and VAL group. Then the left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP) of myocardial infarction (MI) of the right common carotid artery in the right common carotid artery were measured by using the BL-420F bio-functional experimental system in each group. The contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in myocardium and the activities of Na + -K + -ATPase and Ca2 + -ATPase in cardiomyocytes were determined by oxidation assay and thiobarbituric acid chromogenic assay. Results: VAL could reduce the systolic blood pressure in MI rabbits but not in MI rabbits (P> 0.05), but decrease the end diastolic pressure (P <0.01) The decrease of SOD in rabbits restored and increased significantly (P <0.01). VAL reduced the activity of Na + -K + -ATPase and Ca2 + -ATPase in MI rabbits and increased (P <0.05). CONCLUSION: VAL may improve myocardial infarction (MI) via stabilizing the anti-lipid peroxidation of cell membrane and enhancing the clearance of oxygen free radicals and the activity of Na + -K + -ATPase ATPase and Ca2 + -AT-Pase in myocardium after MI.