Division of Cardiothoracic Surgery, Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center of Emory University Hospital Midtown, Emory University School of Medicine, Atlanta, Georgia 30308-2225, USA.
J Cardiovasc Med (Hagerstown). 2013 Mar;14(3):206-13. doi: 10.2459/JCM.0b013e32835cecc6.
The treatment of reperfusion injury requires measures beyond timely reperfusion. Conventional postconditioning (PostC) of ischemic tissues offers a strategy to reduce reperfusion injury, but its adoption is challenged by requiring access and imposing additional ischemia to the ischemic organ. Generating protective signals by PostC in a tissue remote from the target organ such as the limb, i.e. remote PostC (rPostC), may present an alternative approach to exerting endogenous tissue protection. Because rPostC is only recently reported, the fundamental biology of rPostC is not well understood, and studies to date are largely observational. rPostC has been observed to reduce ischemia-reperfusion injury experimentally in heart, kidney, brain and skeletal muscle in multiple species, including rat, rabbit and pig. Both necrosis and apoptosis are reduced. As in remote ischemic preconditioning, rPostC requires a transfer or communication of protective factors or signals through humoral and/or neural pathways. Triggers of target organ protection include G-protein-coupled receptor ligands, metabolites of ischemia, or small thermolabile molecules. Some evidence suggests that reperfusion injury salvage kinases may be involved in rPostC, in agreement with both preconditioning and conventional PostC. Clinical studies investigating improvements in clinical outcomes or biomarkers with rPostC are encouraging.
再灌注损伤的治疗需要采取超越及时再灌注的措施。缺血组织的传统后处理（PostC）提供了一种减少再灌注损伤的策略，但由于需要进入和对缺血器官施加额外的缺血，其应用受到了挑战。通过在远离靶器官（如肢体）的组织中产生 PostC 的保护信号，即远程 PostC（rPostC），可能是发挥内源性组织保护的一种替代方法。由于 rPostC 最近才被报道，因此 rPostC 的基本生物学尚未得到很好的理解，迄今为止的研究主要是观察性的。rPostC 已被观察到在多种物种（包括大鼠、兔和猪）的心脏、肾脏、大脑和骨骼肌中减少实验性缺血再灌注损伤。坏死和凋亡均减少。与远程缺血预处理一样，rPostC 需要通过体液和/或神经途径转移或传递保护因子或信号。靶器官保护的触发因素包括 G 蛋白偶联受体配体、缺血代谢物或小的热敏分子。一些证据表明，再灌注损伤挽救激酶可能参与 rPostC，这与预处理和传统 PostC 一致。研究 rPostC 对临床结局或生物标志物改善的临床研究令人鼓舞。
