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目的研究大鼠心肺复苏后神经细胞线粒体通透性转换孔(MPTP)的变化规律。方法建立窒息联合冰氯化钾致大鼠心搏骤停、心肺复苏(CA/CPR)的动物模型,断头后提纯大脑皮层组织内线粒体,采用分光光度法测定线粒体MPTP在不同时相的开放程度。结果心肺复苏后大鼠神经细胞线粒体功能明显受损,恢复自主循环(ROSC)后神经细胞MPTP持续处于开放状态,开放程度具有时间依赖性,具体表现为在ROSC后6h以内开放程度保持低水平,6h以后开始迅速大量开放,直至12h开放程度达到最大,但并没有一直维持这一水平,而是在ROSC后24h开放程度略有缩小,表明线粒体开始收缩,至48h开放程度再次加大,72hMPTP明显缩小,但未达到正常水平。结论CA/CPR后大鼠线粒体MPTP出现明显规律性改变,复苏后12h以内可能是改善复苏后脑功能的最佳治疗窗。
Objective To study the changes of mitochondrial permeability transition pore (MPTP) in rat neurons after cardiopulmonary resuscitation. Methods Animal model of asphyxiation combined with ice-induced potassium chloride in cardioplegia and cardiopulmonary resuscitation (CA / CPR) was established. The mitochondria in cerebral cortex tissue were purified after decapitation, and the mitochondrial MPTP was determined by spectrophotometry in different phases degree. Results The function of mitochondria in rat neurons after cardiopulmonary resuscitation was significantly impaired. The MPTP of neurons remained open after recovery of autonomic circulation (ROSC), and the degree of opening was time-dependent. The results showed that MPTP maintained at a low level within 6 hours after ROSC, 6h after the opening of a large number of rapid open until 12h to reach the maximum degree of openness, but did not maintain this level, but in the 24 hours after ROSC open slightly reduced, indicating mitochondria began to shrink, open again to 48h, 72h MPTP significantly Shrink, but did not reach the normal level. Conclusion The mitochondrial MPTP changes obviously after CA / CPR. Within 12 hours after resuscitation, MPTP may be the best therapeutic window to improve brain function after resuscitation.