Vascular remodeling and proliferation of smooth muscle cells through the release of endothelin-1 (ET-1) in the subacute and chronic phases of ARDS occludes the pulmonary vasculature, further increasing PVR and the accumulation of interstitial edema, contributing to the development of PH (Moloney and Evans, 2003). This evidence concerns the gene EDN1 and acute respiratory distress syndrome.