Mechanical ventilation triggers the manifestation of lung injury and pre-injured lungs are more susceptible. Ventilation-induced abnormalities of alveolar surfactant are involved in injury progression. The effects of mechanical ventilation on the surfactant system might be different in healthy compared to pre-injured lungs. In the present study, we investigated the effects of different positive end-expiratory pressure (PEEP) ventilations on the structure of the blood–gas barrier, the ultrastructure of alveolar epithelial type II (AE2) cells and the intracellular surfactant pool (= lamellar bodies, LB). Rats were randomized into bleomycin-pre-injured or healthy control groups. One day later, rats were either not ventilated, or ventilated with PEEP = 1 or 5 cmH₂O and a tidal volume of 10 ml/kg bodyweight for 3 h. Left lungs were subjected to design-based stereology, right lungs to measurements of surfactant proteins (SP−) B and C expression. In pre-injured lungs without ventilation, the expression of SP-C was reduced by bleomycin; while, there were fewer and larger LB compared to healthy lungs. PEEP = 1 cmH₂O ventilation of bleomycin-injured lungs was linked with the thickest blood–gas barrier due to increased septal interstitial volumes. In healthy lungs, increasing PEEP levels reduced mean AE2 cell size and volume of LB per AE2 cell; while in pre-injured lungs, volumes of AE2 cells and LB per cell remained stable across PEEPs. Instead, in pre-injured lungs, increasing PEEP levels increased the number and decreased the mean size of LB. In conclusion, mechanical ventilation-induced alterations in LB ultrastructure differ between healthy and pre-injured lungs. PEEP = 1 cmH₂O but not PEEP = 5 cmH₂O ventilation aggravated septal interstitial abnormalities after bleomycin challenge.

机械通气会引发肺损伤的表现，受伤前的肺更容易受到影响。通气引起的肺泡表面活性剂异常与损伤进展有关。与受伤前的肺部相比，机械通气对表面活性剂系统的影响在健康人中可能有所不同。在本研究中，我们研究了不同呼气末正压通气 (PEEP) 通气对血气屏障结构、肺泡 II 型 (AE2) 细胞超微结构和细胞内表面活性剂池（= 层状体）的影响， 磅）。将大鼠随机分为博莱霉素预损伤组或健康对照组。一天后，大鼠要么不通气，要么用 PEEP = 1 或 5 cmH ₂通气O 和 10 毫升/公斤体重的潮气量 3 小时。左肺接受基于设计的体视学，右肺接受表面活性蛋白 (SP-) B 和 C 表达的测量。在没有通气的损伤前肺中，博来霉素降低了SP-C的表达；同时，与健康的肺相比，LB 更少但更大。PEEP = 1 cmH ₂由于间隔间质体积增加，博莱霉素损伤肺的 O 通气与最厚的血气屏障有关。在健康的肺中，增加 PEEP 水平会降低平均 AE2 细胞大小和每个 AE2 细胞的 LB 体积；而在受伤前的肺中，AE2 细胞的体积和每个细胞的 LB 在整个 PEEP 中保持稳定。相反，在受伤前的肺中，增加 PEEP 水平会增加 LB 的数量并减少 LB 的平均大小。总之，机械通气引起的 LB 超微结构改变在健康肺和受伤前肺之间有所不同。PEEP = 1 cmH ₂ O 但不是 PEEP = 5 cmH ₂ O 通气加重博来霉素激发后的间隔间质异常。