Liver Ischemic Preconditioning Mechanism

Background: IPC(ischemia preconditioning) is a process where by a briefischemic episode confers a state of protection against subsequent long-termischemia-reperfusion injury. The exact mechanism is not well known,especially therole of NO(nitric oxide),OFR(oxygen free radical) are controversy. The current studywas designed to evatulate the effect of NO,OFR on HIRI(hepaticischemia-reperfusion injury) rabbit liver after IPC,and research the mechanism of IPCto rabbit liver.Methods:Using hepatic ischemia-reperfusion models, 15 healthy japan rabbbitswas divided into three groups randomly: control group(A,n=5), HIRI gruop(Bn=5), IPC group(C=5). After IPC and HIRI, observe the differences of NOx, MDA,SOD and ALT levels in blood, as well as the differences of NOx, MDA, SOD levels inHIRI gruop; while MDA and ALT levels of plasma werelower than thosein HIRIgroup, and the levels of NOx had not significant differences between IPC and Controlgroup; In hepatic tissue, the levels of SOD, NOx was higher than those in HIRI group,while the levels of MDA is lower than thosein HIRI group; Abnormal morphologicalchanges of liver cellsin IPC group were ameliorated remarkably during HIRI.Conclusions: Improved OFR and attenuated NO is the primary causes forHIRI; IPC protect HIRI liver through improving NO level and attenuating OFR level.