Objective To investigate the early responses and roles of Pre-B-cell colony-enhancing factor (PBEF)during acute lung injury(au)induced by seawater-immersion after open chest trauma.Method Sixteen dogs randomly divided(random number)into seawater group(SG)and control group(CG).Blood samples were collected at 0,2,4,6,8 h after Irauma.Broncho-alveolar lavage fluid(BALF)and lung tissue were collected at 8 h after trauma.The levels of inflammatory cytokines(IL-1β,IL-8 and vWF)in the plasma and PBEF in the plasma,BALF and lung tissue were measured with ELISA Kit.The plasma osmotic pressue,electrolyte concentralion from plasma and total protein concentration from BALF and plasma were measured.And then,the correlations among the PBEF,plasma osmotic pressue,and inflammatory cytokines were analyzed.All data were analyzed by SPSS 10.0 software.Results Comparedwith"CG",the levels of PBEFfrom the plasm,BALF and hmg tissue at 8 h after trauma were significantly increased in"SG",P＜0.O1[in plasma:(3014.16±883.47)vs.(1060.94±251.08);in BALF:(1373.35±102.53)vs.(997.77±70.31);in lung tissue:(1455.22±71.74)vs.(921.43±118.13),pg/mL];The peak of the levels of PBEF in the plasma were significant different both occuring timing(4 h vs.6 h)and values[(3204.56±604.21)vs.(1220.86±191.30)]between in"SG"and "CG"(P＜0.05).IL-1β,IL-8 and vWF from the plasma showed same changes.Significant correlations were observed between the level of PBEF and PPI,the level of PBEF and plasma osmotic pressure.The correlation coefficients were 0.489(PBEF vs.PPI),0.549(PBEF vs.IL-1β),0.496(PBEF vs.IL-8),O.465(PBEF vs.vWf),respectively.Conclusions These results indicated that PBEF was one of the major inflammatory cytokines released in the early phase of acute lung injury induced by seawater-immersion after open chest trauma,and played an important role in the development of it.Monitoring the hvels of PBEF may offer a significant information to predict the ALI.%目的 探讨胸部开放伤合并海水浸泡致急性肺损伤(AlJ)早期前B细胞集落刺激因子(PBEF)水平及意义.方法 16只犬致胸部开放伤后随机(随机数字法)分成对照组(n=8,单纯胸部开放伤)和海水组(n=8,胸部开放伤后5min内经伤口灌人海水35 mL/kg),10min内闭合伤口,制成au模型.伤后0,2,4,6,8 h取动脉和静脉血,8 h取支气管肺泡灌洗液(BALF)和肺组织标本.检测血浆及BALF中总蛋白浓度、血浆渗透压和电解质浓度;ELISA方法测血浆炎症因子IL-1β、IL-8和内皮细胞损伤标志物vWF水平,以及血浆、BALF和肺组织中PBEF水平;PBEF与血浆渗透压、炎症因子行简单相关分析.采用SPSS 10.0统计软件分析数据.结果 海水组动物血浆、BALF和肺组织中PBEF水平较对照组明显升高,差异具有统计学意义(P＜0.01):伤后8 h海水组PBEF水平较对照组显著升高[血浆内:(3014.16±883.47)vs.(1060.94±251.08);BALF内:(1373.35±102.53)vs.(997.77±70.31);肺组织内:(1455.22±71.74)vs.(921.43±118.13),pg/mL];血浆内PBEF水平峰值海水组出现在伤后4 h(3204.56±604.21),对照组出现在伤后6 h(1220.86±191.30),且二者峰值差异具有统计学意义(P＜0.05).血浆IL-1β,IL-8和vWF水平变化与PBEF一致,海水组较对照组明显升高,差异有统计学意义(P＜0.01).PBEF水平升高与炎症因子和血浆渗透压明显正相关(P＜0.01),其相关系数分别为0.489(PBEF vs.PPI),0.549(PBEF vs.IL-1β),0.496(PBEF vs.IL-8),0.465(PBEF vs.vWf).结论 胸部开放伤合并海水浸泡致au早期PBEF水平进行性升高,与海水高渗有关.PBEF参与au炎症病理过程,可以作为胸部开放伤海水浸泡致au早期较为敏感的监测指标之一.
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