Open AccessCell Injuries of the Blood‐Air Barrier in Acute Lung Injury Caused by Perfluoroisobutylene Exposure
Author(s) -
Meng Ge,
Zhao Jian,
Wang HeMei,
Ding RiGao,
Zhang XianCheng,
Huang ChunQian,
Ruan JinXiu
Publication year - 2010
Publication title -
journal of occupational health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 59
ISSN - 1348-9585
DOI - 10.1539/joh.l9047
Subject(s) - bronchoalveolar lavage , apoptosis , lung , pathology , pulmonary edema , western blot , medicine , alveolar wall , edema , necrosis , chemistry , andrology , biochemistry , gene
Cell Injuries of the Blood‐Air Barrier in Acute Lung Injury Caused by Perfluoroisobutylene Exposure: Ge M eng , et al . Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, PR ChinaObjectives To investigate the complete process of cell injuries in the blood‐air barrier after perfluoroisobutylene (PFIB) exposure. Methods Rats were exposed to PFIB (140 mg/m 3 ) for 5 min. The pathological changes were evaluated by lung wet‐to‐dry weight ratio, total protein concentration of bronchoalveolar lavage fluid and HE stain. Ultrastructural changes were observed by transmission electron microscope. Apoptosis was detected by in situ apoptosis detection. Changes of actin in the lung tissue were evaluated by western blot assay. Results No significant pulmonary edema or increased permeability was observed within the first 4 h, post PFIB exposure. However, inflammatory cell infiltration and alveolar wall thickening were observed from 2 h. Destruction of the alveoli constitution integrity, edema and protein leakage were observed at 8 h. The injuries culminated at 24 h and then recovered gradually. The ultrastructural injuries of alveolar type I epithelial cells, alveolar type II epithelial cells and pulmonary microvascular endothelial cells were observed at 30 min post PFIB exposure. Some injuries were similar to apoptosis. Compared with control, more serious injuries were observed in PFIB‐exposed rats after 30 min. At 8 h, some signs of cell necrosis were observed. The injuries culminated at 24 h and then ameliorated. The number of apoptotic cells abnormally increased at 30 min post PFIB exposure, the maximum appeared at 24 h, and then ameliorated gradually. Western blot analysis revealed that the level of actin in the lung showed no significant changes within the first 4 h post PFIB exposure. However, it decreased at 8 h, reached a nadir at 24 h, and then recovered gradually. Conclusions The pathological processes were in progress persistently post PFIB exposure. The early injuries probably were the result of the direct attack of PFIB and the advanced injuries probably arose from the inflammatory reaction induced by PFIB.