AIM:To investigate the relationship between donor liver cold preservation,lung surfactant (LS) changes and acute lung injury (ALI) after liver transplantation.METHODS:Liver transplantation models were estab-lished using male Wistar rats.Donor livers were pre-served in University of Wisconsin solution at 4 ℃ for different lengths of time.The effect of ammonium pyr-rolidinedithiocarbamate (PDTC) on ALI was also detect-ed.All samples were harvested after 3 h reperfusion.The severity of ALI was evaluated by lung weight/body weight ratio,lung histopathological score,serum nitric oxide (NO) and endothelin (ET)-1 levels,lung tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels.Lung surfactants (LSs) were determined by micellar electrokinetic capillary chromatography.RESULTS:With extended donor liver cold preservation time (CPT),lung histopathological scores,serum ET-1 levels,lung weight/body weight ratio and the level of TNF-α and IL-1β in lung were increased significantly in the 180-min group compared with the sham group (3.16 ± 0.28 vs 1.12 ± 0.21,P < 0.001;343.59 ± 53.97 vs 141.53 ± 48.48,P < 0.001;0.00687 ± 0.00037 vs 0.00557 ± 0.00056,P < 0.001;17.5 ± 3.0 vs 1.3 ± 0.3,P < 0.001;10.8 ± 2.3 vs 1.8 ± 0.4,P < 0.001),but se-rum NO levels decreased remarkably (74.67 ± 10.01 vs 24.97 ± 3.18,P < 0.001).The expression of lung phos-phatidylcholine (PC),phosphatidylethanolamine (PE),phosphatidylinositol (PI) and phosphatidylserine (PS) increased when CPT was < 120 min,and decreased when CPT was > 180 min (PC:1318.89 ± 54.79 vs 1011.18 ± 59.99,P < 0.001;PE:1504.45 ± 119.96 vs 1340.80 ± 76.39,P=0.0019;PI:201.23 ± 34.82 vs 185.88 ± 17.04,P=0.2265;PS:300.43 ± 32.95 vs 286.55 ± 55.55,P=0.5054).All these ALI-associated indexes could be partially reversed by PDTC treatment.CONCLUSION:Prolonged CPT could induce or inhibit the expression of LSs at the compensation or decom-pensation stage,and some antioxidants (e.g.,PDTC) may reverse the pathological process partially. To investigate the relationship between donor liver cold preservation, lung surfactant (LS) changes and acute lung injury (ALI) after liver transplantation. METHODS: Liver transplantation models were estab-lished using male Wistar rats. Donor livers were pre-served in University of Wisconsin solution at 4 ° C for different lengths of time. The effect of ammonium pyr-rolidinedithiocarbamate (PDTC) on ALI was also detect-ed. All of the samples were harvested after 3 h reperfusion. The severity of ALI was evaluated by lung weight / body weight ratio, lung histopathological score, serum nitric oxide (NO) and endothelin (ET) -1 levels, lung tumor necrosis factor (TNF) -α and interleukin (IL) -1β levels were determined by micellar Electrokinetic capillary chromatography .RESULTS: With extended donor liver cold preservation time (CPT), lung histopathological scores, serum ET-1 levels, lung weight / body weight ratio and the level of TNF-α and IL-1β in lung were increased significantly in th e 180-min group compared with the sham group (3.16 ± 0.28 vs 1.12 ± 0.21, P <0.001; 343.59 ± 53.97 vs 141.53 ± 48.48, P <0.001; 0.00687 ± 0.00037 vs 0.00557 ± 0.00056, P <0.001; 17.5 ± 3.0 but se-rum NO levels decreased remarkably (74.67 ± 10.01 vs 24.97 ± 3.18, P <0.001). The expression of lung phos- Phosphatidylethanolamine (PE), phosphatidylinositol (PI) and phosphatidylserine (PS) increased when CPT was <120 min and decreased when CPT was> 180 min (PC: 1318.89 ± 54.79 vs 1011.18 ± 59.99, P <0.001; PE: 1504.45 ± 119.96 vs 1340.80 ± 76.39, P = 0.0019; PI: 201.23 ± 34.82 vs 185.88 ± 17.04, P = 0.2265; PS: 300.43 ± 32.95 vs 286.55 ± 55.55, P = 0.5054) be under a reversed phase of PDTC treatment. CONCLUSION: Prolonged CPT could induce or inhibit the expression of LSs at the compensation or decom-pensation stage, and some antioxidants (eg, PDTC) may reverse the pathological pro cess partially