1. According to the Starling resistor model of the pulmonary circulation, the pulmonary hypertension of oleic acid lung injury, an experimental model close to the early stage of clinical ARDS, primarily results from an increased vascular closing pressure which exceeds Pla and becomes the effective outflow pressure of the pulmonary circulation. Therefore, calculated pulmonary vascular resistance should be interpreted cautiously during haemodynamic investigations in patients with ARDS. 2. Part of this increased vascular closing pressure is functional. During acute lung injury pulmonary vasomotor tone can be reduced by vasodilators, or increased by cyclooxygenase inhibitors and almitrine. 3. Pulmonary vasodilation due to infused vasodilators usually impairs gas exchange in ARDS. 4. There is evidence that HPV is altered during ARDS. Drugs capable of enhancing the efficacy of HPV could improve gas exchange. If proven safe in the future, cyclooxygenase inhibitors and almitrine are interesting compounds to be tested in ARDS.