Research Progress Of Cardioprotection Induced By Sevoflurane Preconditioning In Myocardial Ischemia-reperfusion Injury

Ischemia-repurfusion injury(IRI) is ischemia injury of tissue and organs after restoration of blood flow after transient ischemia and caused further reversible or irreversible cell damage.It is an important factor to affect the success and prognosis of cardiac surgery.The sevoflurane preconditioning of cardium is a hotpot in recent years for it will reduce myocardial IRI,but the exact pathogenesis is still unclear.Here we summarize and analyze it.The mechanism of myocardial IRI:①The overproduction of ROS.ROS peroxidates membrane lipid and increases its permeability which enlarges the inflow of Ca+,all these causing intracellular calcium overload and the mitochondria dysfunction;ROS causes destruction of DNA;ROS causes inhibition of protein and enzymes;ROS induces the induction of inflammatory factors.②ntracellular calcium overload. Intracellular calcium overload induces the production of ATP,promotes mitochondria dysfunction and actives a variety of Ca2+dependent degradative enzymes.which finally cause cell damage.Intracellular calcium overload and the generation of ROS are in reciprocal causation,they play an impeotant role in myocardial IRI.③The mediators of inflammation generated in repurfusion induce aggregation and adhesion of leukocytes,resulting in mechanical obstruction and uncontrolled inflammatory reaction.④Apoptosis.The sevoflurane preconditioning can improve myocardial contractility, reduce arrhythmia, improve cardiac function and myocardial perfusion, reduce infarct size. Its mechanisms are as follows.⑤The role of ROS.The small amount of ROS generated by sevoflurane preconditioning promote the synthesis of NO,increase the activation of PKC, and promote the generation of glutathione peroxidase, CAT and SOD,and increase the expression of GST.It plays a protective effect.②Promote mito-K.ATP channels opening.Mito-KATP channels’open can reduce the generation of ROS.stable mitochondrial transmembrane potentinal,adjust the volume of mitochondrial matrix.reduce mitochondrial calcium overload and suppress the opening of MPTP,thereby reducing the mitochondrial injury in reperfusion.③ Regulate the expression of apoptotic gene.Sevoflurane preconditioning can upregulate the expression of Bcl-2gene while lowering the expression of Bax gene.supress the activation of caspase family,inhibite the expression of Fas and FasL,thereby reducing apoptosis.④The sevoflurane preconditioning can inhibit the activation of neutrophils and other inflammatory cells,and reduce the expression of IL,TNF-a,et al.⑥Reduced NF-κB’s activity.⑦Activation of PI3K/Akt signaling pathway.The activation of PI3K/Akt pathway can inhibite the activation of NF-κB, reduce the opening of MPTP, promote the synthesis of NO and increase the ratio of Bcl-2/Bax,thereby to play a positive role in myocardial protection.The commonly used animal model in myocardial IRI are rats:in vivo models and in vitro models.Here we introduce the most used methods to making these two models.Finally,with the review and relevant literature as the background,we design the research directions and methods in future.