Tátrai E, Brozik M, Adamis Z, Merétey K, Ungváry G
National Institute of Occupational Health, Budapest, Hungary.
J Appl Toxicol. 1996 Mar-Apr;16(2):129-35. doi: 10.1002/(SICI)1099-1263(199603)16:2<129::AID-JAT316>3.0.CO;2-C.
Cellulose after a single intratracheal dose (15 mg per animal) brought about fibrosing granulomatous alveobronchiolitis and an increase of IgA production in the bronchoalveolar lavage. Fibrosing alveolitis showed moderate progression as a function of time. With different morphological methods, injury of type I pneumocytes and the incomplete repair of type II pneumocytes were detected. The damage of the alveolar epithelium initiated and activated a series of processes that led to definite pulmonary alterations: pulmonary fibrosis leading to the disintegration of the alveolo-capillary morphological functional unit.
单次气管内给药(每只动物15毫克)后,纤维素引发了纤维化性肉芽肿性肺泡支气管炎,并导致支气管肺泡灌洗中IgA产生增加。纤维化性肺泡炎随时间呈中度进展。通过不同的形态学方法,检测到I型肺细胞损伤和II型肺细胞修复不完全。肺泡上皮损伤引发并激活了一系列导致明确肺部改变的过程:肺纤维化导致肺泡-毛细血管形态功能单位解体。