AIM:To investigate the effects and mechanisms of ischemicpreconditioning(IPC)on the ischemia/reperfusion(I/R)injuryof liver cirrhosis in rats and the effect of IPC on P-selectinexpression in hepatocytes.METHODS:Forty male SD rats with liver cirrhosis wererandomly divided into sham operation group(SO group),ischemia/reperfusion group(I/R group),ischemicpreconditioning group(IPC group),L-Arginine preconditioninggroup(APC group),L-NAME preconditioning group(NPCgroup),eight rats in each group.Hepatocellular viability wasassessed by hepatic adenine nucleotide level and energycharge(EC)determined by HPLC,ALT,AST and LDH in serummeasured by auto- biochemical analyzer and bile output.The expression of P-selectin in the liver tissue was analyzedby immunohistochemical technique.Leukocyte count inischemic hepatic lobe was calculated.RESULTS:At 120 min after reperfusion,the level of ATPand EC in IPC and APC groups was higher than that in I/Rgroup significantly.The increases in AST,ALT and LDH wereprevented in IPC and APC groups.The livers produced morebile in IPC group than in I/R group during 120 min afterreperfusion(0.101±0.027 versus 0.066±0.027 ml/g liver,P=0.002).There was a significant difference between APCand I/R groups,(P=0.001).The leukocyte count in livertissues significantly increased in I/R group as compared withSO group(P<0.05).The increase in the leukocyte countwas prevented in IPC group.Administration of L-arginineresulted in the same effects as in IPC group.However,inhibition of NO synthesis(NPC group)held back thebeneficial effects of preconditioning.Significant promotionof P-selectin expression in hepatocytes in the I/R groupwas observed compared with the SO group(P<0.01).IPCor L-arginine attenuated P-selectin expression remarkably(P<0.01).However,inhibition of NO synthesis enhanced P-selectin expression(P<0.01).The degree of P-selectinexpression was positively correlated with the leukocytecounts infiltrating in liver(r=0.602,P=0.000).CONCLUSION:IPC can attenuate the damage induced byI/R in cirrhotic liver and increase the ischemic tolerance ofthe rats with liver cirrhosis.IPC can abolish I/R induced leukocyte adhesion and infiltration by preventing post-ischemic P-selectin expression in the rats with liver cirrhosisvia a NO-initiated pathway. AIM: To investigate the effects and mechanisms of ischemic preconditioning (IPC) on the ischemia / reperfusion (I / R) injuryof liver cirrhosis in rats and the effect of IPC on P-selectine expression in hepatocytes. METHODS: Forty male SD rats with liver cirrhosis wererandomly The rats were divided into sham operation group (SO group), ischemia / reperfusion group (I / R group), ischemic preconditioning group (IPC group), L-Arginine preconditioning group (APC group) group.Hepatocellular viability was measured by hepatic adenine nucleotide level and energycharge (EC) determined by HPLC, ALT, AST and LDH in serummeasured by auto-biochemical analyzer and bile output. The expression of P-selectin in the liver tissue was analyzed by immunohistochemical technique. Leukocyte count in ischemic hepatic lobe was calculated .RESULTS: At 120 min after reperfusion, the level of ATP and EC in IPC and APC groups was higher than that in I / Rgroup significantly. Increases in AST, ALT and LDH were prevented in IPC and APC groups. The livers produced more than one in IPC group than in I / R group during 120 min afterreperfusion (0.101 ± 0.027 versus 0.066 ± 0.027 ml / g liver, P = 0.002). There was a significant difference between APCand I / R groups, (P = 0.001). The leukocyte count in livertissues significantly increased in I / R group as compared withSO group (P <0.05). The increase in the leukocyte count was prevented in IPC group. Administration of L-arginineresulted in the Inhibition of NO synthesis (NPC group) held back the benefits of preconditioning. Significant promotion of P-selectin expression in hepatocytes in the I / R group was observed compared with the SO group (P <0.01). The degree of P-selectin expression was positively correlated with the leukocytecounts infiltrating in liver (r <0.05). IPCor L-arginine attenuated P-selectin expression was remarkably (P <0.01) = 0.602, P = 0.000) .CONCLUSION: IPC can att enuate the damage induced by I / R in cirrhotic liver and increase the ischemic tolerance of the rats with liver cirrhosis. IPC can abolish I / R induced leukocyte adhesion and infiltration by preventing post-ischemic P-selectin expression in the rats with liver cirrhosisvia a NO- initiated pathway.