全氟异丁烯单次暴露诱发小鼠急性肺损伤的长期效应

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...

Long-term effect of a single perfluoroisobutylene exposure induced acute lung injury in mice

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.