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目的观察缺血后处理在减轻家兔心肌缺血再灌注损伤中的作用,并探讨其可能机制。方法将32只健康成年雄性家兔随机分为4组(每组8只),分别为假手术组(Sham)、缺血再灌组(I/R)、缺血后处理组(I-postC)、缺血后处理+5-羟葵酸组(I-postC+5-HD)。采用结扎左冠前降支30 min/复灌60 min的方法复制心肌缺血再灌注损伤模型。观察并比较各组动物在缺血前、缺血30 min、复灌60 min时LVSP和LVEDP值、血浆CK活性和MDA含量,测定心肌缺血和梗死面积。结果在复灌60 min时,与I/R组相比,I-postC组LVSP明显升高(P<0.05);LVEDP明显降低(P<0.05);血浆CK活性明显降低(P<0.05);血浆MDA含量明显降低(P<0.05);心肌梗死面积明显减小(P<0.05)。比较I/R组和I-postC+5-HD组LVSP、LVEDP、血浆CK活性和MDA含量未见明显差异,梗死面积也未见差异。结论缺血后处理可通过开放线粒体ATP敏感性钾通道,减轻心肌缺血再灌注损伤。
Objective To observe the effect of ischemic postconditioning on alleviating myocardial ischemia-reperfusion injury in rabbits and to explore its possible mechanism. Methods Thirty-two healthy adult male rabbits were randomly divided into 4 groups (8 in each group), sham group, I / R group and I-postC group ), Ischemic postconditioning + 5-hydroxalic acid group (I-postC + 5-HD). The models of myocardial ischemia-reperfusion injury were duplicated by ligating left anterior descending coronary artery for 30 min / reperfusion for 60 min. The LVSP and LVEDP, the activity of CK and the content of plasma MDA were observed and compared before ischemia, 30 min ischemia, 60 min reperfusion. The myocardial ischemia and infarct area were measured. Results Compared with I / R group, LVSP in I-postC group was significantly increased (P <0.05), LVEDP was significantly decreased (P <0.05), and plasma CK activity was significantly decreased (P <0.05) Plasma MDA content was significantly lower (P <0.05); myocardial infarction area was significantly reduced (P <0.05). LVSP, LVEDP, plasma CK activity and MDA content in I / R group and I-postC + 5-HD group were not significantly different, but no difference in infarct size. Conclusion Ischemic postconditioning can relieve myocardial ischemia-reperfusion injury by opening mitochondrial ATP-sensitive potassium channels.