CAJ | 학술논문

目的：研究尼卡地平对快速上浮脱险致减压病动物模型肺组织损伤的影响。方法雄性SD大鼠60只，随机分为3组，每组20只。实验组于进舱前0．5 h给予尼卡地平50 mg/kg灌胃，对照组于进舱前0．5 h给予相同体积的生理盐水灌胃，空白对照组仅放于加压舱内相同时间不做加压处理。空气以2t/7指数速率加压至1．5 MPa，停留4 min后匀速减压至常压出舱。出舱后0．5 h观察大鼠存活率、肺组织病理，通过ELISA检测IL1-β和TNF-α表达量，并通过Western印迹检测肺组织半胱天冬蛋白酶（ caspase ）3表达的改变。结果对照组发病率和死亡率分别为80％和50％，实验组发病率和死亡率分别为100％和80％。两组存活动物的肺组织病理均可见肺泡、肺间质出血，肺间质增宽。实验组TNF-α较正常组有明显升高，而IL1-β未见明显改变。尼卡地平处理后前半胱天冬蛋白酶（pro-caspase）3无显著改变，但裂解半胱天冬蛋白酶（cleaved-caspase）3明显增高。结论减压前使用尼卡地平对快速上浮脱险致减压病造成的肺损伤有促进作用，并促使了炎症加重和细胞凋亡增加。
목적：연구니잡지평대쾌속상부탈험치감압병동물모형폐조직손상적영향。방법웅성SD대서60지，수궤분위3조，매조20지。실험조우진창전0．5 h급여니잡지평50 mg/kg관위，대조조우진창전0．5 h급여상동체적적생리염수관위，공백대조조부방우가압창내상동시간불주가압처리。공기이2t/7지수속솔가압지1．5 MPa，정류4 min후균속감압지상압출창。출창후0．5 h관찰대서존활솔、폐조직병리，통과ELISA검측IL1-β화TNF-α표체량，병통과Western인적검측폐조직반광천동단백매（ caspase ）3표체적개변。결과대조조발병솔화사망솔분별위80％화50％，실험조발병솔화사망솔분별위100％화80％。량조존활동물적폐조직병리균가견폐포、폐간질출혈，폐간질증관。실험조TNF-α교정상조유명현승고，이IL1-β미견명현개변。니잡지평처리후전반광천동단백매（pro-caspase）3무현저개변，단렬해반광천동단백매（cleaved-caspase）3명현증고。결론감압전사용니잡지평대쾌속상부탈험치감압병조성적폐손상유촉진작용，병촉사료염증가중화세포조망증가。
Objective To study the effect of nicardipine on fast floating escape induced lung injury in animal models with decompression sickness .Methods Sixty male SD rats were randomly and evenly divided into three groups:blank control, control and nicardipine groups .The nicardipine group was given nicardipine 50 mg/kg orally 0.5 h before entrance.In the control group, rats were given an equal volume of saline 0.5 h before entrance.The blank control group only stayed in the vehicle without any pressurized procedure .The air was pressurized at the 2t/7 exponential rate to 1.5 Mpa which was maintained for 4 min, and then uniformly decompressed to atmospheric pressure .The extravehicular survival and lung pathology were observed in rats after 0.5 h, IL1-βand TNF-αexpression levels were detected by ELISA , and the Caspase 3 expression in lung tissue was detected by Western blot .Results The incidence and mortality rate were 80%and 50%respectively in control group ,and 100%and 80%in the experimental group .The surviving animals in the two groups suffered from alveolar and interstitial lung hemorrhage , with widened interstitial lung .IL1-βin the experimental group was significantly higher than in the normal control group , while TNF-αhad no significant change .After nicardipine treatment pro-caspase 3 did not change significantly , but cleaved-caspase 3 increased significantly .Conclusion Nicardipine can aggravate lung injury caused by fast floating escape-induced decompression sickness if used before decompression.