Chabot F, Mitchell J A, Gutteridge J M, Evans T W
Service des Maladies Respiratoires et Reanimation Respiratoire, CHU Nancy-Brabois, Vandoeuvre-les-Nancy, France.
Eur Respir J. 1998 Mar;11(3):745-57.
The acute respiratory distress syndrome (ARDS) in adults is associated with a wide variety of precipitating factors, often not directly involving the lung, and has an associated mortality of 50-80%. ARDS is almost invariably associated with sepsis, either as an initiating factor or as a secondary complication, which increases the expression of a number of cytokines impacting upon several cellular systems. Specifically, activation of neutrophils sequestered in the pulmonary circulation by this process, causes the release of free radicals and reactive oxygen species (ROS), increasingly regarded as key substances modulating the endothelial dysfunction and disruption responsible for the principal clinical manifestations of the syndrome. Here we discuss briefly the pathophysiology of ARDS and its impact upon pulmonary vascular control; the biological origins of free radicals and other ROS involved, the mechanisms of their damaging effects, their contribution to the modification of pulmonary vascular control mechanisms in lung injury and possible therapeutic perspectives.
成人急性呼吸窘迫综合征（ARDS）与多种促发因素相关，这些因素通常并非直接累及肺部，其相关死亡率为50% - 80%。ARDS几乎总是与脓毒症相关，脓毒症既可以是起始因素，也可以是继发并发症，它会增加多种影响多个细胞系统的细胞因子的表达。具体而言，在此过程中，肺循环中滞留的中性粒细胞被激活，会导致自由基和活性氧（ROS）的释放，这些物质越来越被视为调节内皮功能障碍和破坏的关键物质，而内皮功能障碍和破坏正是该综合征主要临床表现的原因。在此，我们简要讨论ARDS的病理生理学及其对肺血管控制的影响；所涉及的自由基和其他ROS的生物学来源、它们的损伤作用机制、它们对肺损伤中肺血管控制机制改变的作用以及可能的治疗前景。
