CAJ | 학술논문

目的探讨常压氧和高压氧暴露对实验鼠肺组织损伤的影响.方法 60只雄性SD大鼠,按数字表法随机分为6组,每组10只,分别暴露于0.10、0.15、0.20、0.25、0.30 MPa 100％氧气中56、20、10、8、6h,暴露于空气的大鼠作为对照组.出舱后检测肺泡灌洗液蛋白含量、白细胞数、肺湿干比、肺组织凋亡蛋白caspase-3表达.结果与对照组比较,0.10 MPa组大鼠肺湿干比、支气管肺泡灌洗液蛋白量及白细胞数、cleaved-caspase-3表达明显增高.随着氧分压的增高,这种改变减弱.与0.10 MPa组相比,高压氧组的肺湿干比、肺泡灌洗液蛋白含量及细胞数、凋亡蛋白含量显著降低.结论炎症和凋亡在常压氧导致的肺型氧中毒起着重要作用,但在高压氧导致的肺型氧中毒中的作用不明显.
목적 탐토상압양화고압양폭로대실험서폐조직손상적영향.방법 60지웅성SD대서,안수자표법수궤분위6조,매조10지,분별폭로우0.10、0.15、0.20、0.25、0.30 MPa 100％양기중56、20、10、8、6h,폭로우공기적대서작위대조조.출창후검측폐포관세액단백함량、백세포수、폐습간비、폐조직조망단백caspase-3표체.결과 여대조조비교,0.10 MPa조대서폐습간비、지기관폐포관세액단백량급백세포수、cleaved-caspase-3표체명현증고.수착양분압적증고,저충개변감약.여0.10 MPa조상비,고압양조적폐습간비、폐포관세액단백함량급세포수、조망단백함량현저강저.결론 염증화조망재상압양도치적폐형양중독기착중요작용,단재고압양도치적폐형양중독중적작용불명현.
Objective Oxygen is often used clinically to treat hypoxia patients,however,prolonged exposure to normobaric oxygen as well as hyperbaric oxygen will induce oxygen toxicity.Our study was designed to explore different manifestations of pulmonary oxygen toxicity (POT) induced by prolonged normobaric and hyperbaric oxygen exposures.Methods Sixty male SD rats were randomly divided into 6 groups and exposed to 0.10、0.15、0.20、0.25 MPa and 0.30 MPa pure oxygen for 56,20,10,8 and 6 hours respectively.Rats exposed to air were used as control.Protein levels and white cell counts in the bronchoalveolar lavage fluid (BALF),wet/dry ratio of the lung and the expression of caspase-3 in lungs were detected after exposure.Results For the 0.10 MPa group,the protein levels and white cell counts in BALF,the wet/dry ratio of lung and the expression of cleaved-caspase-3 all significantly increased,as compared to those of the air group.With the elevation of oxygen partial pressure,these changes tended to decrease.Wet/dry ratio of the lung,protein levels and white cell counts in BALF and the expression of cleaved-caspase-3 all significantly decreased,as compared to those of the 0.10 MPa group.Conclusions Inflammation and apoptosis played an important role in the pathogenesis of normobaric pulmonary oxygen toxicity,however,their role in the pulmonary oxygen toxicity induced by HBO was not so obvious as was observed.