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机构地区:[1]汕头大学医学院第二附属医院麻醉科,广东汕头515041
出 处:《华南国防医学杂志》2015年第11期814-816,823,共4页Military Medical Journal of South China
基 金:广东省医学科研基金项目(A2012403)
摘 要:目的探讨脂氧素A4(Lioxi NA4,LXA4)对兔单肺通气肺损伤的保护作用及其机制。方法健康日本大耳白兔18只,随机分为3组:TLV组、OLV组和LXA组,各6只。TLV组双侧肺机械通气3 h。OLV组插入自制双腔气管导管,右侧肺单肺通气2 h,然后恢复双侧肺通气1 h。LXA组由静脉输入LXA4 2μg/kg,而后实施单肺通气,其余操作同OLV组。实验结束前经股动脉抽血,检测血气分析并计算氧合指数。取各组左右两侧的肺组织,行病理学检查;同时检测各肺组织湿/干重比、髓过氧化物酶(myeloperoxidase,MPO)、丙二醛(malondialdehyde,MDA)超氧化物歧化酶(superoxide dismutase,SOD);酶联免疫吸附剂(enzyme-linked immunosorbent assay,ELISA)测肿瘤转化因子α(tumor necrosis factor alpha,TNF-α)的含量。结果与TLV组比较,氧合指数在OLV组和LXA组均下降(P<0.01),但LXA组比OLV组下降幅度小(P<0.05)。病理学检查显示OLV组两侧均出现炎性改变,且左侧更为严重;LXA组右侧与OLV组相似,而其左侧较OLV组明显改善。各组湿/干重比、MPO、MDA、TNF-含量比较显示OLV组和LXA组左侧明显增高(P<0.01);组间比较,OLV组和LXA组双侧均高于TLV组(P<0.01);LXA组较OLV组双侧均明显降低(P<0.01或0.05),而各组SOD值呈反向变化。结论脂氧素A4对兔单肺通气肺损伤具有一定的保护作用,其作用机制可能与抑制炎症因子合成、减少炎症细胞聚集和缓解氧化应激损伤有关。Objective To study the effects of Lipoxin A4 (LXA4) on one-lung ventilation induced lung injury in a rabbit model.Methods A total of 18 white Japanese rabbits were divided into 3 groups (n = 6 each). The TLV group per- formed two-lung ventilation for 3h. The OLV group performed one-lung ventilation for 2h and two-lung ventilation for the following lh. Lung separation was achieved with an artificial double-lumen tube. The LXA group were pretreated with LXA4 (2 ug/kg, IV. ) prior to one lung ventilation. The blood samples were drawn from femoral artery to get the oxygen- ation indexes. Light microscopic evaluations were performed. Wet/dry ratios (W/D), malondialdehyde (MDA),superox- ide dismutase (SOD), myeloperoxidase (MPO) activity were measured with corresponding methods.TNF-a in lung tis- sues were detected with ELISA.Results Compared with TLV group, the oxygenation of OLV and LXA group were sig- nificantly decreased (P〈0.01). Compared with OLV group, the oxygenation of LXA group were significantly increased (P〈0.05). W/D, MDA, MPO activity and TNF- were significantly increased in left lung compared to right lung in the groups of OLV and LXA (P〈0.01).Compared with TLV group, OLV and LXA groups were significantly elevated (P〈0.01). Compared with OLV group, LXA group was significantly decreased (P 〈0.01 or 0.05). Similar changes of SOD were found in all the groups.Conclusion OLV could cause lung injury by a complex process in the rabbit model. Pretreat- ment with LXA4 could alleviate lung injury by decreasing inflammation factor synthesis, reducing inflammation cell aggre- gates and decreasing oxidative stress reaction.
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