Liver cold preservation induce lung surfactant changes and acute lung injury in rat liver transplantation
Liver cold preservation induce lung surfactant changes and acute lung injury in rat liver transplantation
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DOI：
10.3748/wjg.v18.i4.323
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发表时间：
2012-01-28
影响因子：
4.3
通讯作者：
Lv, Yi
中科院分区：
文献类型：
--
作者：
Jiang, An;Liu, Chang;Lv, Yi
目的：目的：探讨供肝冷保存、肺表面活性物质（LS）变化与肝移植术后急性肺损伤（ALI）的关系。供体肝脏在4 ℃的威斯康星州大学溶液中保存不同的时间长度。观察吡咯烷二硫代氨基甲酸铵（PDTC）对ALI的影响。再灌注3 h后收集所有样本。采用肺重/体重比、肺组织病理学评分、血清一氧化氮（NO）、内皮素（ET）-1水平、肺肿瘤坏死因子（TNO-α）、白细胞介素（IL）-1 β水平评价ALI严重程度。采用胶束电动毛细管色谱法测定肺表面活性物质。随着供肝冷保存时间的延长，肺组织病理学评分、血清ET-1水平、与假手术组相比，180 min组肺重/体重比、肺组织TNF-α和IL-1 β水平显著升高（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），但血清NO水平显著降低（74.67 ± 10.01 vs 24.97 ± 3.18，P < 0.001）。CPT < 120 min时肺磷脂酰胆碱（PC）、磷脂酰乙醇胺（PE）、磷脂酰肌醇（PI）和磷脂酰丝氨酸（PS）表达增加，> 180 min时表达减少（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）。结论：持续CPT可诱导或抑制代偿期或失代偿期LS的表达，并可诱导或抑制某些抗氧化剂（如抗氧化剂、抗氧化剂、抗氧化剂等）的表达。PDTC可部分逆转病理过程。(C)2012年百世登。All rights reserved.
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 established using male Wistar rats. Donor livers were preserved in University of Wisconsin solution at 4 degrees C for different lengths of time. The effect of ammonium pyrrolidinedithiocarbamate (PDTC) on ALI was also detected. 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 (TNO-alpha and interleukin (IL)-1 beta 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-alpha and IL-1 beta 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 serum NO levels decreased remarkably (74.67 +/- 10.01 vs 24.97 +/- 3.18, P < 0.001). The expression of lung phosphatidylcholine (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 decompensation stage, and some antioxidants (e.g., PDTC) may reverse the pathological process partially. (C) 2012 Baishideng. All rights reserved.