Xiao-E Lang, Xiong Wang, Jian-Hua Jin
Journal: Frontiers in bioscience (Landmark edition) 2013;18(1):387-93
PMID: 23276931
Myocardial infarction is responsible for most cardiovascular mortality as well as the pathogenesis of myocardial damage during and after infarction. Efforts are underway to modulate the development of ischemia-reperfusion (I-R) injury. Recently, the protective effect of isoflurane against myocardial I-R injury emerged as a possibility. Nitric oxide, nitric oxide synthases, factors related to energy metabolism, adenosine triphosphate-sensitive potassium channels, phosphatidylinositol-3-kinase and hypoxia-inducible factor1-alpha have been shown to participate in the mechanisms of cardioprotection elicited by isoflurane against I-R injury. In this review, we focus on the mechanisms of cardioprotection offered by isoflurane against I-R injury.
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