摘要目的 研究快速上浮脱险致减压病(DCS)大鼠肺组织转化生长因子β1(TGF.β1)含量的变化.方法 雄性健康SD大鼠68只,采用数字表法随机分为2组:(1)对照组8只,暴露于自然大气环境,自由饮食,不进行任何实验处理.(2)快速上浮脱险致DCS组(DCS组)60只,置于加压舱内进行快速上浮脱险,脱险出舱后0.5、3、6、12、24 h各12只,对各时间点存活动物麻醉后取左、右肺,经相关处理后观察肺组织病理改变并检测TGF-β1含量(以TGF-β1含量/总蛋白浓度表示).结果 肺组织病理损伤在0.5h最重;TGF-β1含量在6h时最低(0.1713 ±0.0195),在24 h时最高(0.1998±0.0537),但与对照组(0.2050±0.0727)比较差异均无统计学意义(P＞0.05).结论 TGF-β1可能在快速上浮脱险致DCS大鼠肺损伤早期的病理过程中并未发挥重要作用.

abstractsObjective To study changes in the cytokine transforming growth factor-β1 (TGF-β1) in the pulmonary tissue of rats as a result of decompression sickness following fast buoyancy ascent escape.Methods Sixty-eight male healthy SD rats were randomly divided into groups.(1) The control group (n =8),exposed to a natural environment with free feeding,were left untreated.(2)The fast buoyancy ascent escape-induced DCS group (n =60) (or simply the DCS group) was placed in the hyperbaric chamber to have fast buoyancy ascent escape.At 0.5 h (hour),3 h,6 h,12 h and 24 h following fast buoyancy ascent escape,pathological changes and contents of TGF-β1 were observed and detected (expressed in contents of TGF-β1/levels of total protein),in all the survived animals.Results Pulmonary injury at 0.5 h was the most obvious after fast buoyancy ascent escape; TGF-β1 lung contents was the lowest at 6 h(0.1713 ±0.0195),and reached peak at 24 h(0.1998 ± 0.0537).No statistical significance could be noticed,when they were compared with those of the control group (0.2050 ± 0.0727) (P ＞ 0.05).Conclusions TGF-β1 might not play any role in the pulmonary pathological process of the development of DCS induced by fast buoyancy ascent escape.