The Basic Science and Molecular Mechanisms of Lung Injury and Acute Respiratory Distress Syndrome.
The Basic Science and Molecular Mechanisms of Lung Injury and Acute Respiratory Distress Syndrome.
复制标题
肺损伤和急性呼吸窘迫综合征的基础科学和分子机制。
DOI：
10.1097/aia.0000000000000177
复制
发表时间：
2018
影响因子：
0.6
通讯作者：
Kaynar AM
中科院分区：
文献类型：
--
作者：
Aranda-Valderrama P;Kaynar AM
急性呼吸窘迫综合征（ARDS）是一种对肺损伤的炎症反应的病理生理状态，包括具有相似终末病理生理特征的直接和间接原因的异质组：血管内皮和肺泡上皮细胞损伤，炎症介质的产生，以及炎性细胞（主要是中性粒细胞）在肺中的积聚。结构性损伤在临床上表现为急性呼吸衰竭综合征，以呼吸困难、继发于气体交换严重受损的进行性动脉低氧血症、肺水肿、肺内出血和呼吸功明显增加为首发症状。3- 7 Ashbaugh、Bigelow和Petty于1967年首次在一组异质性患者中描述了ARDS，并证明了呼气末正压（PEEP）治疗急性呼吸衰竭患者的有益效果。[8]然而，从那时起，ARDS的定义、病理生理学和治疗一直在不断发展。因此，在ARDS背景下对患者进行历史比较是困难的，并且可能不准确。[9]据估计，目前美国每年有20万患者发生这种疾病，死亡率为25%至60%。10、11然而，所研究的所有群组的数据并不同质;
Acute respiratory distress syndrome (ARDS) is a pathophysiological state of inflammatory response to lung injury that encompasses a heterogenous group of direct and indirect causes with similar terminal pathophysiological characteristics: vascular endothelial and alveolar epithelial cell damage, production of inflammatory mediators, and accumulation of inflammatory cells, mainly neutrophils, in the lung. 1, 2 The structural damage is translated clinically into a syndrome of acute respiratory failure that debuts with dyspnea, progressive arterial hypoxemia secondary to severely impaired gas exchange, pulmonary edema, intrapulmonary hemorrhage, and marked increase in ventilatory work. 3–7Ashbaugh, Bigelow, and Petty first described ARDS in 1967 in a heterogenous group of patients and demonstrated the beneficial effect of positive end-expiratory pressure (PEEP) to treat patients with acute respiratory failure. 8 The definition, pathophysiology, and treatment of ARDS, however, has evolved constantly since then. Therefore, a historical comparison of patients within the context of ARDS is difficult and may be imprecise. 9 The current incidence of this disease is estimated as∼ 200,000 patients annually in the United States with mortality rates ranging from 25% to 60%. 10, 11 Yet, the data are not homogenous for all cohorts studied;