Dushianthan Ahilanandan, Grocott Michael P W, Murugan Ganapathy Senthil, Wilkinson Tom M A, Postle Anthony D
National Institute for Health Research (NIHR) Southampton Biomedical Research Centre, University Hospital Southampton National Health System Foundation Trust, Southampton SO16 6YD, UK.
Integrative Physiology and Critical Illness Group, Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton SO16 6YD, UK.
Diagnostics (Basel). 2023 Sep 15;13(18):2964. doi: 10.3390/diagnostics13182964.
Acute respiratory distress syndrome (ARDS) is a major cause of hypoxemic respiratory failure in adults, leading to the requirement for mechanical ventilation and poorer outcomes. Dysregulated surfactant metabolism and function are characteristic of ARDS. A combination of alveolar epithelial damage leading to altered surfactant synthesis, secretion, and breakdown with increased functional inhibition from overt alveolar inflammation contributes to the clinical features of poor alveolar compliance and alveolar collapse. Quantitative and qualitative alterations in the bronchoalveolar lavage and tracheal aspirate surfactant composition contribute to ARDS pathogenesis. Compared to neonatal respiratory distress syndrome (nRDS), replacement studies of exogenous surfactants in adult ARDS suggest no survival benefit. However, these studies are limited by disease heterogeneity, variations in surfactant preparations, doses, and delivery methods. More importantly, the lack of mechanistic understanding of the exact reasons for dysregulated surfactant remains a significant issue. Moreover, studies suggest an extremely short half-life of replaced surfactant, implying increased catabolism. Refining surfactant preparations and delivery methods with additional co-interventions to counteract surfactant inhibition and degradation has the potential to enhance the biophysical characteristics of surfactant in vivo.
急性呼吸窘迫综合征（ARDS）是成人低氧性呼吸衰竭的主要原因，导致需要机械通气且预后较差。表面活性剂代谢和功能失调是ARDS的特征。肺泡上皮损伤导致表面活性剂合成、分泌和分解改变，同时明显的肺泡炎症导致功能抑制增加，二者共同作用导致肺泡顺应性差和肺泡萎陷的临床特征。支气管肺泡灌洗和气管吸出物表面活性剂成分的定量和定性改变促成了ARDS的发病机制。与新生儿呼吸窘迫综合征（nRDS）相比，成人ARDS中外源性表面活性剂的替代研究表明对生存无益处。然而，这些研究受到疾病异质性、表面活性剂制剂、剂量和给药方法差异的限制。更重要的是，对表面活性剂失调的确切原因缺乏机制理解仍然是一个重大问题。此外，研究表明替代的表面活性剂半衰期极短，这意味着分解代谢增加。改进表面活性剂制剂和给药方法，并采取额外的联合干预措施来对抗表面活性剂抑制和降解，有可能增强体内表面活性剂的生物物理特性。
