PDF(Pubmed)
Abstract：
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.
摘要：
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，导致需要机械通气和较差的结果。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改变的组合，分泌，并且由于明显的肺泡炎症而导致的功能抑制作用增加，导致肺泡顺应性差和肺泡塌陷的临床特征。支气管肺泡灌洗和气管抽吸物表面活性剂成分的定量和定性变化有助于ARDS的发病机理。与新生儿呼吸窘迫综合征（nRDS）相比，外源性表面活性剂在成人ARDS中的替代研究表明没有生存益处。然而,这些研究受到疾病异质性的限制，表面活性剂制剂的变化，剂量,和交付方式。更重要的是,缺乏对表面活性剂失调的确切原因的机械理解仍然是一个重要问题。此外，研究表明，替代表面活性剂的半衰期极短，暗示分解代谢增加。用额外的共同干预来抵消表面活性剂抑制和降解的精炼表面活性剂制剂和递送方法具有增强体内表面活性剂的生物物理特性的潜力。
