The molecular basis underlying cardioprotective action of volatile anesthetics on ischemia/reperfusion injury

心肌缺血/再灌流时，心肌细胞内钙动态平衡失调，导致细胞损伤，导致心功能不全，即缺血/再灌流损伤。采用氧化应激或储存操作钙内流(SOCE)介导的钙超载损伤模型，研究了七氟醚对心肌缺血/再灌注损伤保护作用的分子机制。结果发现，七氟醚通过影响兰尼定受体、钠/钙交换器和SOCE通道等多种钙转运途径，保护小鼠心肌细胞免受这些细胞损伤。这些作用似乎对与细胞内钙超载相关的缺血/再灌注损伤产生心脏保护作用。

The disturbance of intracellular Ca2+ homeostasis occurs in myocaridium during ischemia/reperfusion and is responsible for cellular injury leading to cardiac dysfunction, namely ischemia/reperfusion injury. We investigated the molecular mechanisms underlying cardioprotective action of the volatile anesthetic sevoflurane on ischemia/reperfusion injury, using experimental models for Ca2+ overload-induced cellular injuries mediated by oxidative stress or store operated Ca2+ entry (SOCE) process.We found that sevoflurane protects mouse ventricular myocytes against these cellular injuries, presumably by affecting multiple Ca2+ transporting pathway, including ryanodine receptor, Na+/Ca2+ exchanger and SOCE channel. These actions appear to produce the cardioprotection on ischemia/reperfusion injury associated with intracellular Ca2+ overload.