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目的研究ATP敏感性钾通道开放药尼可地尔合用钠钙交换阻滞药KB-R7943对缺血再灌注损伤离体大鼠心脏的作用。方法离体大鼠心脏通过改良Langendorff装置灌流,减少灌流量造成缺血45 min后再灌注2 h建立大鼠心肌缺血再灌注损伤模型,分模型组、尼可地尔组、KB-R7943组、尼可地尔+KB-R7943组,每组10只。TTC染色观察心肌梗死面积,比色法检测冠脉灌流液中过氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,电镜观察心肌超微结构。结果与模型组比较,尼可地尔组和KBR7943组的心肌梗死面积均减小、冠脉灌流液中SOD活性升高、MDA含量下降(P<0.05);与模型组相比,尼可地尔+KB-R7943组的心肌梗死面积、冠脉灌流液中SOD活性和MDA含量改变均非常显著(P<0.01),心肌超微结构损伤减轻,均较尼可地尔组和KB-R7943组有显著改善(P<0.05)。结论尼可地尔合用KB-R7943可显著缩小心肌梗死面积,提高冠脉灌流液中SOD活性,减少MDA含量,减轻心肌超做结构损伤,对缺血再灌注损伤大鼠心脏有保护作用。
Objective To investigate the effect of nicorandil sodium-calcium exchange inhibitor KB-R7943, an ATP-sensitive potassium channel-opening drug, on isolated rat hearts after ischemia-reperfusion injury. Methods The isolated rat hearts were perfused with a modified Langendorff apparatus and the perfusion was reduced to induce ischemia-reperfusion injury in rat models at 45 min after ischemia and 2 h after reperfusion. The rats in model group, nicorandil group and KB-R7943 group , Nicorandil + KB-R7943 group, 10 rats in each group. The area of myocardial infarction was observed by TTC staining. The activity of peroxidase (SOD) and the content of malondialdehyde (MDA) in coronary perfusion fluid were detected by colorimetric method. The myocardial ultrastructure was observed by electron microscope. Results Compared with the model group, the myocardial infarct size in both Nicorandil group and KBR7943 group decreased and the activity of SOD in coronary perfusion fluid increased and the content of MDA decreased (P <0.05). Compared with model group, Nicorandil Myocardial infarction area and the changes of SOD activity and MDA content in coronary artery perfusion fluid of Er + KB-R7943 group were significantly different (P <0.01), and myocardial ultrastructure lesion lessened compared with Nicorandil group and KB-R7943 group There was a significant improvement (P <0.05). Conclusions Nicorandil combined with KB-R7943 can significantly reduce the area of myocardial infarction, increase the activity of SOD in coronary perfusion fluid, decrease the content of MDA, relieve the myocardial ultrastructural damage, and protect the rat heart from ischemia-reperfusion injury.