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Effects of Morphine Postconditioning on Myocardial Ischemia-Reperfusion Injury in Rats in Vivo

机译:吗啡后后处理对体内大鼠心肌缺血再灌注损伤的影响

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Objective.To investigate the effects of morphine postconditioning on Myocardial ischemia reperfusion injury in rats in vivo. Methods. To randomly divide 40 male SD rats equally into 4 groups, including Sham group in which the chest was opened without ligating the left coronary artery, ischemia-reperfusion group (Group I/R), ischemic preconditioning group (Group IPC) and morphine postconditioning group (GroupMOR) in which 0. 3 mg/kg morphine was given intravenously 5 min before reperfusion. The left anterior descending coronary arterys (LAD) of rats in five groups are ligated for 30 minutes and are re-perfused for 90 minutes. Cardiac Apoptosis was determined quantitatively by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) methods. To calculate the concentration of the serum malondialdehyde (MDA) with Thiobarbituric acid (TBA) reaction method and the activity of the superoxide dismutase (SOD) with xanthine oxidase reaction method. Result. Comparing with Group S, the quantity of the cardiac apoptosis in Group I/R, IPC and MOR rised in different levels. Comparing with Group 1/R, the quantity of the cardiac apoptosis in Group IPC and MOR reduced obviously. Comparing with Group 1/R, the concentration of the serum malondialdehyde (MDA) in the other four groups all reduced and the activity of the superoxide dismutase increased. Conclusion. Morphine postconditioning can significantly reduce myocardial apoptosis induced by ischemia-reperfusion injury, reduce myocardial infarct size, decrease the concentration of MDA, and increase the activity of SOD. Therefore, morphine postconditioning has protective effects on myocardial ischemia-reperfusion injury in rats in vivo.
机译:目的。探讨吗啡后后处理对体内大鼠心肌缺血再灌注损伤的影响。方法。将40只雄性SD大鼠随机分成4组,包括假组,其中胸部被打开,而不使左冠状动脉,缺血再灌注组(I / R),缺血预处理组(IPC)和吗啡层后处理组(Groupmor),其中在再灌注前5分钟静脉内给出0. 3mg / kg吗啡。将五组大鼠的左前期下降冠状动脉(LAD)连接30分钟,并重新灌注90分钟。通过末端脱辛核苷酸转移酶介导的DUTP克基末端标记(TUNEL)方法,定量用末端测定心凋亡。用硫氨基甲酸(TBA)反应方法和用黄嘌呤氧化酶反应方法计算血清丙醛(MDA)的浓度和超氧化物歧化酶(SOD)的活性。结果。与S组相比,I / R组中的心脏凋亡的数量在不同层次的IPC和MOR调整。与第1族/ R组相比,IPC和MOR组中心肌细胞凋亡的数量明显减少。与第1族/ R组相比,其他四组血清丙二醛(MDA)的浓度均降低,超氧化物歧化酶的活性增加。结论。吗啡的后处理可以显着减少缺血再灌注损伤的心肌细胞凋亡,减少心肌梗塞大小,降低MDA的浓度,增加了SOD的活性。因此,吗啡后期对体内大鼠心肌缺血再灌注损伤具有保护作用。

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