中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
2014年
3期
174-176
,共3页
王海涛%方以群%攸璞%包晓辰%袁恒荣%张师%马骏%王芳芳
王海濤%方以群%攸璞%包曉辰%袁恆榮%張師%馬駿%王芳芳
왕해도%방이군%유박%포효신%원항영%장사%마준%왕방방
快速上浮脱险%减压病%肺损伤%转化生长因子β1
快速上浮脫險%減壓病%肺損傷%轉化生長因子β1
쾌속상부탈험%감압병%폐손상%전화생장인자β1
Fast buoyancy ascent escape%Decompression sickness%Lung injury%TGF-β1
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.
目的 研究快速上浮脫險緻減壓病(DCS)大鼠肺組織轉化生長因子β1(TGF.β1)含量的變化.方法 雄性健康SD大鼠68隻,採用數字錶法隨機分為2組:(1)對照組8隻,暴露于自然大氣環境,自由飲食,不進行任何實驗處理.(2)快速上浮脫險緻DCS組(DCS組)60隻,置于加壓艙內進行快速上浮脫險,脫險齣艙後0.5、3、6、12、24 h各12隻,對各時間點存活動物痳醉後取左、右肺,經相關處理後觀察肺組織病理改變併檢測TGF-β1含量(以TGF-β1含量/總蛋白濃度錶示).結果 肺組織病理損傷在0.5h最重;TGF-β1含量在6h時最低(0.1713 ±0.0195),在24 h時最高(0.1998±0.0537),但與對照組(0.2050±0.0727)比較差異均無統計學意義(P>0.05).結論 TGF-β1可能在快速上浮脫險緻DCS大鼠肺損傷早期的病理過程中併未髮揮重要作用.
목적 연구쾌속상부탈험치감압병(DCS)대서폐조직전화생장인자β1(TGF.β1)함량적변화.방법 웅성건강SD대서68지,채용수자표법수궤분위2조:(1)대조조8지,폭로우자연대기배경,자유음식,불진행임하실험처리.(2)쾌속상부탈험치DCS조(DCS조)60지,치우가압창내진행쾌속상부탈험,탈험출창후0.5、3、6、12、24 h각12지,대각시간점존활동물마취후취좌、우폐,경상관처리후관찰폐조직병리개변병검측TGF-β1함량(이TGF-β1함량/총단백농도표시).결과 폐조직병리손상재0.5h최중;TGF-β1함량재6h시최저(0.1713 ±0.0195),재24 h시최고(0.1998±0.0537),단여대조조(0.2050±0.0727)비교차이균무통계학의의(P>0.05).결론 TGF-β1가능재쾌속상부탈험치DCS대서폐손상조기적병리과정중병미발휘중요작용.
Objective 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.