吸入麻醉药后处理心肌保护作用机制的研究进展

Pr ogress in research of cardioprotective mechanisms of inhalational anesthetics postcondifioning

背景 吸入麻醉药后处理（inhalational anesthetics postconditioning，APO）是指在缺血后再灌注早期给予一定浓度吸入麻醉药处理。APO具有心肌保护作用，其作用机制目前尚未完全阐明。目的 对APO心肌保护作用机制的研究进展进行回顾和总结。内容 APO的心肌保护的信号转导机制与缺血后处理有很多相似之处，可能是通过刺激心肌产生触发物，活化相关信号通路，激活效应因子，发挥后处理效应。目前研究已证实APO心肌保护作用与激活再灌注损伤补救激酶（reperfusion injury salvage kinase，RISK），抑制再灌注心肌细胞凋亡及线粒体等有关。趋向 APO心肌保护作用机制错综复杂，弄清这些复杂的信号转导机制对于揭示APO效应的原理，促进临床推广具有重要的指导意义。

Background Inhalational Anesthetics Postconditioning （APO） provides inhalational anesthetics of certain concentration at the early stage of reperfusion after myocardial ischemia. APO can apparently protect ischemia/reperfusion myocardium, but its mechanism has not been fully understood. Objective In this paper, we have reviewed the latest progress of the cardioprotective mechanisms of APO. Content The signal transduction of APO is similar to ischemia-induced posteonditioning. APO may stimulate myocardium to produce triggers to activate relevant signaling pathways, and eventually activate effeetors. Multiple studies have demonstrated that activation of reperfusion injury salvage kinase （RISK）, control of cardiocyte apoptosis during reperfusion, opening of mitochondria ATP-sensitive potassium channels （mitoKATP）, mitoehondrial permeability transition pore （mPTP） opening inhibition are involved in the cardioproteetive effects of APO. Trend The cardioproteetive mechanisms of APO are complicated. Fully understand these complex mechanisms of signal transduction will be helpful to illuminate the principle of APO and promote its clinical application.