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目的研究3,4-二-O-甲基-1,2,5,6-四硝酸甘露醇酯(3,4-di-O-methyl-1,2,5,6-D-mannitol tetranitrate,DMMTN)对冠状动脉结扎所致大鼠急性心肌缺血的保护作用及其作用机制。方法以结扎左冠状动脉前降支方法建立大鼠急性心肌缺血模型,建立假手术组、心肌梗死模型组、鲁南欣康组、DMMTN低、中、高剂量(15,30,60 mg.kg-1)组,测定手术后不同时段心电图ST段和T段的抬高;并于手术3 h后硝基四氮唑蓝(NBT)染色法测定心肌梗死面积;测定血清中肌酸激酶(CK)、乳酸脱氢酶(LDH)、丙二醛(MDA)和超氧化物歧化酶(SOD)。结果 DMMTN能显著缩小心肌梗死面积,抑制术后心电图ST段和T段的抬高;能显著降低CK和LDH的活力,以及MDA的含量,同时能显著提高SOD的活力。结论 DMMTN对冠状动脉结扎所致大鼠急性心肌缺血具有显著的保护作用。
Objective To investigate the effects of 3,4-di-O-methyl-1,2,5,6-D-mannitol tetranitrate DMMTN) on acute myocardial ischemia induced by coronary artery ligation in rats. Methods Acute myocardial ischemia model was established by ligation of left anterior descending coronary artery in rats. Sham-operation group, model group of myocardial infarction, Lunanxinkang group, low, medium and high dose of DMMTN (15,30,60 mg. kg-1). The elevation of ST segment and T segment of electrocardiogram were measured at different time points after surgery. The area of myocardial infarction was determined by NBT staining at 3 h after operation. The levels of creatine kinase CK, LDH, MDA and SOD. Results DMMTN could significantly reduce the area of myocardial infarction, inhibit the elevation of ST segment and T segment of postoperative electrocardiogram, reduce the activity of CK and LDH and the content of MDA significantly, and also increase the activity of SOD significantly. Conclusion DMMTN has a significant protective effect on acute myocardial ischemia induced by coronary artery ligation in rats.