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本实验在大鼠离体心脏灌注模型上,模拟心肌缺血再灌注过程(旷置30分钟,再灌注45分钟),结果发现:再灌注后,心脏频发室颤,组织水肿明显,脂质过氧化终产物丙二醛较正常时显著增加,冠脉流出液中乳酸脱氢酶呈一持续高水平释放,心肌组织ATP酶活性明显下降。再灌注开始后给予超氧化物歧化酶(SOD)。能够减轻以上心肌再灌注性损伤现象。这一结果提示:1)活性氧参与了心肌再灌注损伤现象的发生。2)再灌注开始后给予SOD仍有明显疗效,这为临床上在再灌注开始后应用SOD提供了一定的实验依据。
Myocardial ischemia-reperfusion (mock 30 minutes, reperfusion 45 minutes) was simulated in isolated rat heart perfusion model. The results showed that after reperfusion, the heart had frequent ventricular fibrillation and tissue edema, The malondialdehyde (MDA) in the end-product peroxidase increased significantly compared with the normal one. Lactate dehydrogenase in coronary effluent was continuously released at a high level and the activity of ATPase in myocardial tissue was significantly decreased. After reperfusion, superoxide dismutase (SOD) was given. Can reduce the phenomenon of myocardial reperfusion injury. This result suggests: 1) reactive oxygen species involved in the occurrence of myocardial reperfusion injury. 2) After the beginning of reperfusion, there is still a significant effect of giving SOD, which provides a certain experimental basis for clinical application of SOD after reperfusion.