Experimental study on the action and mechanism of delayed protection of ischemic preconditioning on liver ischemia/reperfusion injury in rats

Objective To investigate the likelihood of ischemic preconditioning (IPC) inducing delayed protection against liver ischemia/reperfusion injury in rats, and determine whether this protection works through mitochondrial ATP-sensitive potassium (mitoKATP) channels. Methods Four groups of SD rats (n=8 each) were pretreated with: 5-min period of liver ischemia (IPC group), diazoxide(DE group), IPC plus 5-hydroxydecanoate (IPC+5-HD group) and saline(control group). Twenty-four hours later, the pretreated rats were subjected to 60 min sustained liver ischemia followed by 180 min reperfusion. All rats were subjected to 70% liver ischemia. An additional the fifth group of rats was set(sham group), in which only anesthesia and laparotomy was performed twice. Finally, blood and liver samples were obtained to determine the biochemistry and pathology of the liver. Results The activities of alanine aminotransferase and lactic dehydrogenase, content of malondialdehyde and level of W/D were higher (P 0.01) and the activities of superoxide dismutase were lower (P 0.01) in C group than those in S group. There were also severe morphologic damages in C group. All of the liver injury indexes in IPC group and DE group were better than those in C group (P 0.05 or P 0.01). IPC+5-HD group had the adverse change, contrasted with IPC group (P 0.05 or P0.01). Conclusion IPC can lessen hepatic ischemia/ reperfusion injury through delayed protection due to increased activity of SOD and improves liver microcir-culation, which is correlated with the opening of mitoKATP channels.