| Literature DB >> 29742448 |
Katharine L Hamlington1, Bradford J Smith2, Celia M Dunn3, Chantel M Charlebois3, Gregory S Roy3, Jason H T Bates4.
Abstract
Understanding how the mechanisms of ventilator-induced lung injury (VILI), namely atelectrauma and volutrauma, contribute to the failure of the blood-gas barrier and subsequent intrusion of edematous fluid into the airspace is essential for the design of mechanical ventilation strategies that minimize VILI. We ventilated mice with different combinations of tidal volume and positive end-expiratory pressure (PEEP) and linked degradation in lung function measurements to injury of the alveolar epithelium observed via scanning electron microscopy. Ventilating with both high inspiratory plateau pressure and zero PEEP was necessary to cause derangements in lung function as well as visually apparent physical damage to the alveolar epithelium of initially healthy mice. In particular, the epithelial injury was tightly associated with indicators of alveolar collapse. These results support the hypothesis that mechanical damage to the epithelium during VILI is at least partially attributed to atelectrauma-induced damage of alveolar type I epithelial cells.Entities:
Keywords: Acute respiratory distress syndrome; Alveolar epithelial injury; Lung function measurement; Mechanical ventilation; Scanning electron microscopy
Mesh:
Year: 2018 PMID: 29742448 PMCID: PMC5986619 DOI: 10.1016/j.resp.2018.05.004
Source DB: PubMed Journal: Respir Physiol Neurobiol ISSN: 1569-9048 Impact factor: 1.931