Aso Y, Yoneda K, Kikkawa Y
Lab Invest. 1976 Dec;35(6):558-68.
Pulmonary changes induced by bleomycin were investigated in mice by using light and electron microscopy and by phospholipid analysis of the alveolar washings. The damage began in the endothelium of capillaries and was accompanied by interstitial edema and an appearance of enlarged macrophages along with hypertrophy of type II epithelial cells. This condition was followed by degeneration of type I cells. The denuded epithelium appeared to be repaired by two different mechanisms. In areas away from the bronchioles, division of existing type II cells and subsequent transformation into type I cells appeared to be the pattern of epithelial repair. In areas near the bronchiole, downgrowth of bronchiolar undifferentiated cells and subsequent maturation of these cells to type II and type I cells appeared to be prominent. Biochemically, total phospholipids and disaturated lecithin in the alveolar wash increased along with the increase of the alveolar lining layer and the hypertrophy of type II cells. This was considered to be consistent with the view that the hyperactive type II cells secreted more surfactant in the early phase of the experiment.
通过光学显微镜和电子显微镜以及对肺泡灌洗液进行磷脂分析，研究了博来霉素诱导的小鼠肺部变化。损伤始于毛细血管内皮，伴有间质水肿，出现巨噬细胞增大以及II型上皮细胞肥大。随后是I型细胞变性。裸露的上皮似乎通过两种不同机制修复。在远离细支气管的区域，现有II型细胞分裂并随后转化为I型细胞似乎是上皮修复的模式。在细支气管附近区域，细支气管未分化细胞向下生长并随后成熟为II型和I型细胞似乎很突出。生化方面，随着肺泡衬里层增加和II型细胞肥大，肺泡灌洗液中的总磷脂和二饱和卵磷脂增加。这被认为与实验早期II型细胞过度活跃分泌更多表面活性剂的观点一致。
