• Hong Xie, Jing Zhang, Jiang Zhu, Li-xin Liu, Mario Rebecchi, Su-mei Hu, and Chen Wang.
• Department of Anesthesiology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, China.
• Acta Pharmacol. Sin. 2014 Dec 1; 35 (12): 1504-13.

AimTo investigate the role of extracellular signal-regulated kinases (ERKs) in sevoflurane post-conditioning induced cardioprotection in vitro.MethodsIsolated rat hearts were subjected to 30 min ischemia followed by 120 min reperfusion (I/R). Sevoflurane post-conditioning was carried out by administration of O2-enriched gas mixture with 3% sevoflurane (SEVO) for 15 min from the onset of reperfusion. Cardiac functions, myocardial infarct size, myocardial ATP and NAD(+) contents, mitochondrial ultrastructure, and anti-apototic and anti-oncosis protein levels were measured.ResultsSevoflurane post-conditioning significantly improved the heart function, decreased infarct size and mitochondria damage, and increased myocardial ATP and NAD(+) content in the I/R hearts. Furthermore, sevoflurane post-conditioning significantly increased the levels of p-ERK and p-p70S6K, decreased the levels of porimin, caspase-8, cleaved caspase-3, and cytosolic cytochrome c in the I/R hearts. Co-administration of the ERK1/2 inhibitor PD98059 (20 μmol/L) abolished the sevoflurane-induced protective effects against myocardial I/R.ConclusionSevoflurane post-conditioning protects isolated rat hearts against myocardial I/R injury and inhibits cell oncosis and apoptosis via activation of the ERK1/2 pathway.

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