Ware Lorraine B
Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
Semin Respir Crit Care Med. 2006 Aug;27(4):337-49. doi: 10.1055/s-2006-948288.
Since the adult respiratory distress syndrome was first described substantial progress has been made in understanding the pathogenesis of this complex syndrome. This review summarizes our current understanding of the pathophysiology of what is now termed the acute respiratory distress syndrome (ARDS) and its less severe form acute lung injury (ALI), with an emphasis on cellular and molecular mechanisms of injury that may represent potential therapeutic targets. Although it is difficult to synthesize all of these abnormalities into a single, unified, pathogenetic pathway, a theme that emerges repeatedly is that of imbalance, be it between pro- and anti-inflammatory cytokines, oxidants and antioxidants, procoagulants and anticoagulants, neutrophil recruitment and activation and mechanisms of neutrophil clearance, or proteases and protease inhibitors. Future therapies aimed at restoring the overall balance of cytokines, oxidants, coagulants, and proteases may ultimately be successful where therapies that target individual cytokines or other mediators have not.
自从成人呼吸窘迫综合征首次被描述以来，在理解这一复杂综合征的发病机制方面已经取得了实质性进展。本综述总结了我们目前对现在所称的急性呼吸窘迫综合征（ARDS）及其较轻形式急性肺损伤（ALI）病理生理学的理解，重点关注可能代表潜在治疗靶点的损伤细胞和分子机制。尽管很难将所有这些异常整合到单一、统一的发病途径中，但反复出现的一个主题是失衡，无论是促炎和抗炎细胞因子之间、氧化剂和抗氧化剂之间、促凝剂和抗凝剂之间、中性粒细胞募集和激活以及中性粒细胞清除机制之间，还是蛋白酶和蛋白酶抑制剂之间。旨在恢复细胞因子、氧化剂、凝血剂和蛋白酶整体平衡的未来疗法，在针对个别细胞因子或其他介质的疗法未取得成功的情况下，最终可能会取得成功。
