中文摘要：

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。

英文摘要：

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 typesⅠ and Ⅲ on the wall of vessel and bronchi were severely damaged,but considerable amount of collagen typeⅢ 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.