Pulmonary hypertension due to increased pulmonary vascular resistance, and hypoxaemia based on an elevated intrapulmonary shunt are important pathophysiological features of the adult respiratory distress syndrome (ARDS). Systemically infused vasodilators reduce pulmonary hypertension but also decrease mean systemic arterial pressure and impair pulmonary gas exchange because of their global vasodilatory effects on the systemic and pulmonary circulation. Recently, inhaling low concentrations of the gas nitric oxide (NO), an important endothelium-derived relaxing factor which is rapidly inactivated by binding to haemoglobin, has been shown to induce selective vasodilatation of ventilated lung regions. Thus, inhaled NO reduces pulmonary hypertension in severe ARDS and improves arterial oxygenation by redistributing blood flow away from areas with intrapulmonary shunt to areas with a normal ventilation/perfusion ratio.