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在ＡＲＤＳ发病过程中，ＥＴ－１产生增多，清除减少，因而其水平升高。ＥＴ－１激活嗜中性粒细胞，导致肺血管内皮通透性增加，促进肺水肿的发生。
In the pathogenesis of ARDS, ET-1 production increased, decreased clearance, and thus its level increased. ET-1 activates neutrophils, leading to increased permeability of the pulmonary vascular endothelium, promoting pulmonary edema.