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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。
Objective To investigate the effect of nicardipine on the lung injury in animal models of decompression sickness caused by rapid ascent and desorption. Methods Sixty male Sprague-Dawley rats were randomly divided into three groups of 20 rats each. The experimental group was given nicardipine 50 mg / kg orally 0.5 h before feeding, and the same volume of saline was given 0.5 h before the infusion in the control group. The blank control group was placed in the pressurization tank only at the same time and did not do Pressurized. The air was pressurized to 1.5 MPa at an exponential rate of 2 t / 7, and after 4 min of residence, the air was depressurized at constant pressure to atmospheric pressure. The survival rate and lung histopathology of rats were observed after 0.5 h. The expressions of IL1-β and TNF-α were detected by ELISA. The expression of caspase 3 in lung tissue was detected by Western blotting. Results The morbidity and mortality in the control group were 80% and 50%, respectively. The morbidity and mortality in the experimental group were 100% and 80% respectively. Survival of the two groups of lung tissue pathology can be seen in alveoli, interstitial lung bleeding, pulmonary interstitial widened. The level of TNF-αin the experimental group was significantly higher than that of the normal group, while the level of IL1-β was not changed obviously. There was no significant change in pre-caspase 3 after nicardipine treatment, but cleaved-caspase 3 was significantly increased. Conclusions The use of nicardipine before depressurization can promote the lung injury caused by decompression sickness caused by rapid ascent and descent and promote the increase of inflammation and apoptosis.