Abstract
Background Inhaled anesthetics postconditioning （APO） exerts potent protection against myocardial ischemia/ reperfusion （l/R） injury. This cardioprotection of APO involves complex cell signaling pathways. Objective Here we retrospectively summarized cell signaling pathways and downstream effectors in volatile anesthetic postconditioning-induced cardioprotection. Contents A great deal of studies show that APO exerts cardioprotection against I/R injury through activating reperfusion injury salvage kinase pathways, the following protein kinase C and nitric oxide cascades, as well as inhibiting reactive oxygen species overproduction, cellular Ca2 ＋ overload, and mitochondrial apoptosis. Trend To clarify the key cell signaling pathway and downstream effectors in the cardioprotection of APO is helpful to find a new potential target for treatment of myocardial I/R injury, which is important to ontimize the APO strateaw a~ainst myocardial I/R injury and has translational medical meaninz. Key words: Inhaled anesthetics; Postconditioning; Cell signaling pathway; Myicardial ischemia/reperfusion
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