The pathways activated by post-conditioning may converge on the mitochondria, in particular on the mitochondrial permeability transition pore. We sought to characterize the inhibition status of the mitochondrial permeability transition early after the post-conditioning maneuver and before long reperfusion was established. We observed that post-conditioning maneuvers applied to isolated rat hearts, after a prolonged ischemia and before reperfusion, promoted cardiac mechanical function recovery and maintained mitochondrial integrity. These effects were evaluated by mitochondrial swelling, calcium transport, and NAD(+) content measurements; the improvements were established before restoring a long lasting reperfusion period. Mitochondrial integrity was associated with a diminution in oxidative stress, since carbonylation of proteins was prevented and aconitase activity was preserved in the post-conditioned hearts, implying that ROS might mediate mitochondrial dysfunction and mPTP opening. In addition, we found that cytochrome release was significantly abolished in the post-conditioned heart, in contrast with conventionally reperfused hearts.

中文翻译：

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后适应性心脏中氧化应激与线粒体功能之间的关系。

通过后处理激活的途径可能会聚集在线粒体上，尤其是在线粒体通透性过渡孔上。我们力求表征后调节操作后和建立长再灌注之前的线粒体通透性转变的抑制状态。我们观察到，在长时间的缺血后和再灌注之前，对分离的大鼠心脏进行后处理操作，可促进心脏机械功能的恢复并保持线粒体的完整性。通过线粒体肿胀，钙转运和NAD（+）含量测量来评估这些影响。在恢复长期持续的再灌注期之前已建立了改进措施。线粒体完整性与氧化应激的降低有关，由于可以防止蛋白质的羰基化，并在后置条件的心脏中保留乌头酸酶的活性，这表明ROS可能介导线粒体功能障碍和mPTP的开放。此外，我们发现，与常规再灌注心脏相比，后调节心脏的细胞色素释放显着消除。