Objective To investigate the effect of hydrogen inhalation on acute lung injury after hemorrhagic shock in rats.Methods Twenty-four adult male Sprague-Dawley (SD) rats were equally randomized into three groups:sham operation group,model group and hydrogen-treatment group.Pressure-controlled hemorrhagic shock and resuscitation model was reproduced by blood-letting for 1 hour followed by fluid replacement for 2 hours.The rats in model group received a mixture of 50％ oxygen-50％ nitrogen during the process.The rats in hydrogen-treatment group received inhalation of a mixture of 2％ hydrogen-48％ nitrogen-50％ oxygen 10 minutes before fluid replacement till the end of resuscitation.The arterial blood samples were collected for the measurement of arterial partial pressure of oxygen (PaO2) before exsanguination,1 hour after shock,1 hour and 2 hours after fluid replacement.Blood and lung tissues were collected at the end of experiment,and tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels in plasma,lung wet/dry weight ratio (W/D),malondialdehyde (MDA) content,superoxide dismutase (SOD) and myeloperoxidase (MPO) activity in the lung tissue were determined.The lung tissue was subjected to pathological examination.Results At the end of fluid replacement,compared with model group,hydrogen could significantly reduce pulmonary edema (lung W/D ratio:4.72 ± 0.12 vs.4.94 ± 0.14,P＜0.05),inhibit oxidative stress [MDA (nmol/mg):0.55 ± 0.09 vs.0.72± 0.08,P＜O.05],enhance antioxidant activity [SOD activity (U/mg):79.53 ± 14.33 vs.59.55 ± 9.07,P＜0.05],reduce the release of pro-inflammatory cytokines [TNF-α (ng/L):55.58 ± 10.06 vs.66.58 ± 5.17; IL-6 (ng/L):23.00 ± 2.77 vs.27.09 ± 2.46,P＜ 0.05] and inhibit neutrophil infiltration [MPO (U/g):1.05 ± 0.18 vs.1.40 ± 0.14,P＜0.05].It alleviated the damage to lung tissue,and then improved the lung function [PaO2 (mm Hg,1 mm Hg=0.133 kPa):146.3 ± 22.1 vs.123.6 ± 16.0,P＜0.05].Conclusion Hydrogen treatment can alleviate acute lung injury as a result of hemorrhagic shock and resuscitation.%目的 探讨氢气对失血性休克复苏诱导大鼠急性肺损伤的影响.方法 按照随机数字表法将24只雄性SD大鼠均分为假手术组、模型组、氢气治疗组,采用缺血1h再灌注2h制备大鼠压力控制型失血性休克复苏模型,模型动物在制模过程中吸入50％氧气-50％氮气,氢气治疗组再灌注开始前10 min改为吸入2％氢气-48％氮气-50％氧气直至复苏结束.于放血前、休克1h和再灌注1h、2h取血,检测动脉血氧分压(PaO2)；实验结束时取血和肺组织标本,检测血浆中肿瘤坏死因子-α(TNF-α)及白细胞介素-6(IL-6)水平,以及肺湿/干质量比值(W/D)、肺组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性,并观察肺组织病理学改变.结果 再灌注结束后,与模型组相比,氢气治疗组可明显减轻肺水肿(肺W/D比值:4.72±0.12比4.94±0.14,P＜0.05),抑制氧化应激[MDA (nmol/mg):0.55±0.09比0.72±0.08,P＜0.05],增强抗氧化酶活性[SOD(U/mg):79.53±14.33比59.55±9.07,P＜ 0.05],减少促炎因子释放[TNF-α (ng/L):55.58±10.06比66.58±5.17,IL-6(ng/L):23.00±2.77比27.09±2.46,P＜0.05]及中性粒细胞浸润[MPO(U/g):1.05±0.18比1.40±0.14,P＜0.05],减轻肺组织病理学损伤,改善肺功能[PaO2(mm Hg,1 mm Hg=0.133 kPa):146.3±22.1比123.6±16.0,P＜ 0.05].结论 氢气治疗可减轻失血性休克复苏诱导的急性肺损伤.
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