CAJ | 학술논문

目的探讨全氟异丁烯( PFIB)单次暴露诱发急性肺损伤的长期效应.方法 70只雄性小鼠暴露于全氟异丁烯130 mg·m-3 5 min.10只小鼠于暴露后24 h评价肺水肿程度.其余小鼠分别在PFIB暴露后2,4,6,8,12和16周,应用HE染色和天狼星红染色分别观察肺组织的病理变化和胶原沉积,测定肺及血浆中羟脯氨酸含量.结果 PFIB暴露后24 h诱发了严重肺水肿.染毒后2周肺组织仍然观察到肺泡腔内炎性细胞浸润、蛋白质渗出、肺泡隔增厚、肺间质和肺泡水肿.血管壁和支气管壁Ⅰ和Ⅲ型胶原损伤严重,但肺泡壁Ⅲ型胶原大量沉积.与正常对照组相比,肺组织羟脯氨酸含量明显下降(P＜0.01),但血浆中羟脯氨酸含量比明显上升(P＜0.01),这种变化趋势一直持续到第6周,从第8周逐渐恢复正常,到第16周染毒组与正常组相比无显著性差异.从第4周开始,肺组织损伤和血管壁和支气管壁胶原损伤逐渐恢复,肺泡壁Ⅲ型胶原逐渐吸收.16周后,肺组织病理损伤及胶原变化几乎恢复正常.结论 PFIB单次暴露后,早期血管壁和支气管壁胶原严重破坏,但后期无肺纤维化发生.
목적 탐토전불이정희( PFIB)단차폭로유발급성폐손상적장기효응.방법 70지웅성소서폭로우전불이정희130 mg·m-3 5 min.10지소서우폭로후24 h평개폐수종정도.기여소서분별재PFIB폭로후2,4,6,8,12화16주,응용HE염색화천랑성홍염색분별관찰폐조직적병리변화화효원침적,측정폐급혈장중간포안산함량.결과 PFIB폭로후24 h유발료엄중폐수종.염독후2주폐조직잉연관찰도폐포강내염성세포침윤、단백질삼출、폐포격증후、폐간질화폐포수종.혈관벽화지기관벽Ⅰ화Ⅲ형효원손상엄중,단폐포벽Ⅲ형효원대량침적.여정상대조조상비,폐조직간포안산함량명현하강(P＜0.01),단혈장중간포안산함량비명현상승(P＜0.01),저충변화추세일직지속도제6주,종제8주축점회복정상,도제16주염독조여정상조상비무현저성차이.종제4주개시,폐조직손상화혈관벽화지기관벽효원손상축점회복,폐포벽Ⅲ형효원축점흡수.16주후,폐조직병리손상급효원변화궤호회복정상.결론 PFIB단차폭로후,조기혈관벽화지기관벽효원엄중파배,단후기무폐섬유화발생.
OBJECTIVE To investigate whether the pulmanary fibrosis formed after a single PFIB exposure.METHODS A total of 70 male mice were exposed to PFIB 130 mg·m-3 for 5 min.Pulmonary edema of 10 mice was evaluated by lung indices at 24 h after PFIB exposure.Pathological changes and collagen deposition were detected by hematoxylin and eosin (HE) and Sirius red stainings in the other mice,changes in collagen content in lungs and plasma by measuring the respective hydroxyproline content at 2,4,6,8,12 and 16 weeks after PFIB exposure.RESULTS Severe pulmonary edema was observed at 24 h after PFIB exposure.At day 14 after PFIB exposure,inflammatory cell infiltration,alveolar septum thickening,interstitial and alveolar edema and protein leakage were noticed.Collagens types Ⅰ and Ⅲ on the wall of vessel and bronchi were severely damaged,but considerable amount of collagen type Ⅲ deposited on the alveolar wall.The content of hydroxyproline considerably decreased in the lungs but increased significantly in the plasma up to six weeks.Hydroxyproline in lungs and plasma began to recover at the end of 8 weeks,and then returned to normal.At 16 weeks,they recovered to normal level.At the end of 4 weeks,the lung lesions and the collagens at the wall of vessel and bronchi began to recover gradually; collagen typeⅢ at the alveolar wall was gradually absorbed,too.At 16 weeks,the lungs almost recovered to normal level.CONCLUSION At earlier phase after PFIB exposure,the excessive collagens destruction in lungs is observed,but no pulmonary fibrosis forms at the later phase.