Cardiac Preconditioning by Anesthetic Agents: Roles of Volatile Anesthetics and Opioids in Cardioprotection

Cardiac preconditioning is the most potent and consistently reproducible method of protecting heart tissue against myocardial ischemia-reperfusion injury. This review discussed about the signaling and amplification cascades from either ischemic preconditioning stimulus or pharmacological preconditioning stimulus, the putative end-effectors and the mechanisms involved in cellular protection. The pharmacological preconditioning induced by volatile anesthetics and opioids is very similar to the ischemic preconditioning. It includes activation of G-protein-coupled receptors, multiple protein kinases and ATP-sensitive potassium channels (KATP channels). Volatile anesthetics prime the activation of the sarcolemmal and mitochondrial KATP channels, which are the putative end-effectors of preconditioning, by stimulation of adenosine receptors and subsequent activation of protein kinase C (PKC) and by increased formation of nitric oxide and free oxygen radicals. Similarly, opioids activate δ- and κ-opioid receptors leading to activation of PKC. The open state of the mitochondrial KATP channel and sarcolemmal KATP channel ultimately induces cytoprotection by decreasing Ca2+ overload in the cytosol and mitochondria.