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目的:研究线粒体钙激活钾通道在大鼠肢体远距缺血预处理(RPC)对缺血再灌注心肌损伤保护中的作用机制。方法:分离大鼠右下肢股动脉,结扎5min,松开复灌5min,共4个循环。取出心脏悬挂于Langen-dorff灌流装置,全心停灌30min,复灌120min。分离心肌细胞线粒体,电镜观察心肌线粒体结构变化;检测不同处理组线粒体膜电位、线粒体内NOS、Mn-SOD、Ca2+含量的变化。结果:与单纯缺血复灌组相比,RPC组和钙激活钾通道开放剂NS1619组心脏复灌后心肌线粒体损伤减轻,内外膜结构较完整;心肌细胞线粒体膜电位增加(P<0.01)、Mn-SOD含量增高(P<0.01),NOS含量降低(P<0.01)、Ca2+含量下降(P<0.01);与RPC组相比,RPC与钙激活钾通道开放阻断剂Paxilline联合组各指标有明显差异(P<0.01)。结论:心肌线粒体钙激活钾通道可能通过维持线粒体膜电位,减少心肌复灌期线粒体NO生成和Ca2+含量升高,提高线粒体抗氧化能力而在肢体RPC心肌保护发挥作用。
AIM: To investigate the mechanism of mitochondrial calcium-activated potassium channels in the protection of distal limb ischemic preconditioning (RPC) on myocardial ischemia-reperfusion injury. Methods: The right fellow femoral artery was isolated, ligation 5min, release reperfusion 5min, a total of 4 cycles. Remove the heart hanging in Langen-dorff perfusion device, stop the whole heart 30min, reperfusion 120min. The mitochondria of myocardial cells were isolated and the mitochondrial structure was observed by electron microscope. The changes of mitochondrial membrane potential and contents of NOS, Mn-SOD and Ca2 + in mitochondria of different groups were detected. Results: Compared with the ischemia-reperfusion group, the mitochondrial membrane damage in the group of NS1619 and the RPC group and the calcium-activated potassium channel opener NS1619 group were relieved. The mitochondrial membrane potential was increased (P <0.01) (P <0.01), and the content of Ca2 + decreased (P <0.01). Compared with the RPC group, the levels of Mn-SOD and Paxilline combined with calcium-activated potassium channel blockers There was a significant difference (P <0.01). Conclusion: The calcium-activated potassium channel in myocardial mitochondria may play a protective role in the myocardial protection of RPC by maintaining the mitochondrial membrane potential and decreasing the mitochondrial NO production and Ca2 + content during myocardial reperfusion.