Department of Medicine, University of California, San Francisco, San Francisco, California.
Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California.
Semin Respir Crit Care Med. 2019 Feb;40(1):31-39. doi: 10.1055/s-0039-1683996. Epub 2019 May 6.
Acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure caused by noncardiogenic pulmonary edema. Despite five decades of basic and clinical research, there is still no effective pharmacotherapy for this condition and the treatment remains primarily supportive. It is critical to study the molecular and physiologic mechanisms that cause ARDS to improve our understanding of this syndrome and reduce mortality. The goal of this review is to describe our current understanding of the pathogenesis and pathophysiology of ARDS. First, we will describe how pulmonary edema fluid accumulates in ARDS due to lung inflammation and increased alveolar endothelial and epithelial permeabilities. Next, we will review how pulmonary edema fluid is normally cleared in the uninjured lung, and describe how these pathways are disrupted in ARDS. Finally, we will explain how clinical trials and preclinical studies of novel therapeutic agents have further refined our understanding of this condition, highlighting, in particular, the study of mesenchymal stromal cells in the treatment of ARDS.
急性呼吸窘迫综合征（ARDS）是一种由非心源性肺水肿引起的急性呼吸衰竭综合征。尽管已经进行了五十年的基础和临床研究，但目前仍没有针对这种疾病的有效药物治疗，治疗仍然主要是支持性的。研究导致 ARDS 的分子和生理机制对于提高我们对这种综合征的认识和降低死亡率至关重要。本综述的目的是描述我们目前对 ARDS 的发病机制和病理生理学的理解。首先，我们将描述肺炎症和肺泡内皮和上皮通透性增加如何导致 ARDS 中肺积水的积聚。接下来，我们将回顾未受损肺中肺积水是如何正常清除的，并描述 ARDS 中这些途径是如何被破坏的。最后，我们将解释新型治疗药物的临床试验和临床前研究如何进一步完善我们对这种情况的理解，特别是强调间充质基质细胞在治疗 ARDS 中的研究。
