Abstract
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.
Highlights
The pulmonary surfactant system plays a critical role in reducing end-expiratory surface tension at the alveolar air–liquid interface as well as in minimizing respiratory workload during inspiration (Bachofen and Schürch 2001)
The alveolar epithelial cells were slim at the thin side of the blood–gas barrier with hardly any signs of injury such as clearance of the cytoplasmic ground substance, blebbing or fragmentation
On the thick side of the blood–gas barrier, which usually contributes 50% of the blood–gas barrier and where the epithelial and endothelial basal laminae are separated by interstitial tissue, the layers of the blood–gas barrier were compact without any signs of an interstitial oedema
Summary
The pulmonary surfactant system plays a critical role in reducing end-expiratory surface tension at the alveolar air–liquid interface as well as in minimizing respiratory workload during inspiration (Bachofen and Schürch 2001). These physiological functions are essential for alveolar micromechanics, defined as the morphological changes of alveoli during the respiratory cycle (Matuszak et al 2020). The intra-alveolar surfactant pool responsible for biophysical and immunological functions can be differentiated from the intra-cellular surfactant pool within the alveolar epithelial type II (AE2) cells (Ochs 2010) Pulmonary surfactant, including both lipids and surfactant proteins, is synthesized, stored and secreted by AE2 cells (Perez-Gil and Weaver 2010; Ochs et al 2020). Mutations in the Abca gene have been shown to result in ultrastructurally abnormal LB which become smaller and more numerous (Beers et al 2017)
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