Gill Sean E, Yamashita Cory M, Veldhuizen Ruud A W
Centre for Critical Illness Research, Lawson Health Research Institute, London, ON, Canada.
Departments of Medicine and Physiology & Pharmacology, Western University, London, ON, Canada.
Cell Tissue Res. 2017 Mar;367(3):495-509. doi: 10.1007/s00441-016-2521-8. Epub 2016 Oct 29.
Acute respiratory distress syndrome (ARDS) is a disease with a variety of causes and is defined by severe hypoxemia. Whereas ARDS carries a mortality of approximately 30 %, patients that survive may ultimately regain near normal pulmonary physiology. The critical pathophysiological processes in ARDS are alveolar barrier dysfunction and overwhelming inflammation. This encompasses damage to the epithelial and endothelial layers, thickening of the interstitial matrix, edema with inactivation of pulmonary surfactant at the alveolar surface and marked inflammation mediated by infiltrating neutrophils and pro-inflammatory macrophages. For patients that survive the disease, these are the critical processes that require repair and remodeling to allow for the recovery of ARDS. As such, the current review focuses on the experimental studies that have begun to elucidate the mechanisms involved in restoring the alveolar barrier following injury.
急性呼吸窘迫综合征（ARDS）是一种病因多样的疾病，其定义为严重低氧血症。尽管ARDS的死亡率约为30%，但存活下来的患者最终可能恢复到接近正常的肺生理状态。ARDS的关键病理生理过程是肺泡屏障功能障碍和过度炎症反应。这包括上皮和内皮细胞层受损、间质基质增厚、肺泡表面肺表面活性物质失活导致的水肿以及由浸润的中性粒细胞和促炎巨噬细胞介导的明显炎症。对于从该疾病中存活下来的患者，这些是需要修复和重塑以实现ARDS恢复的关键过程。因此，本综述聚焦于已开始阐明损伤后恢复肺泡屏障所涉及机制的实验研究。
