• Ge Zhao, Xin Shen, Haiyan Nan, Linfeng Yan, Haikang Zhao, Jun Yu, and Yi Lv.
• Department of Anesthesiology, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, China.
• J. Surg. Res. 2013 Aug 1;183(2):827-34.

BackgroundRemifentanil protects against ischemia/reperfusion (I/R)-induced organ injury, although its underlying mechanism remains elusive. This study was designed to examine the protective effect of remifentanil preconditioning, if any, against hepatic I/R injury in rats and the underlying mechanism involved.Materials And MethodsAdult Sprague-Dawley rats were randomly divided into sham operation (S group), ischemia/reperfusion (I/R group), and remifentanil preconditioning (R group) groups. Rats in the I/R group were subjected to a partial (70%) hepatic ischemia for 45 min, followed by 1 h, 3 h, and 6 h of reperfusion. Rats in the R group received venous injection of remifentanil (2 μg/kg/min) from 30 min prior to hepatic ischemia to the end of ischemia. Hepatic morphology and apoptosis were examined. Markers of liver damage, oxidative stress, and inflammation were evaluated. Mitochondrial function was assessed using mitochondrial membrane potential and appearance of mitochondrial swelling.ResultsCompared with the S group, rats in the I/R group displayed a massive degenerative death in liver tissues and significantly enhanced cell apoptosis. Remifentanil preconditioning significantly reduced I/R-induced hepatocyte apoptosis. In addition, remifentanil protected against I/R-induced mitochondrial swelling and loss of membrane potential. Remifentanil preconditioning inhibited I/R-induced increases in tumor necrosis factor α, intercellular adhesion molecule 1, and nuclear factor κB p65 levels in liver tissues. Remifentanil preconditioning also inhibited the loss in superoxide dismutase and rise in malondialdehyde levels in liver tissues going through I/R injury.ConclusionsOur data revealed that remifentanil preconditioning may turn on multiple cellular pathways in hepatocytes to protect the liver from I/R injury by alleviating hepatic apoptosis.Copyright © 2013 Elsevier Inc. All rights reserved.

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