Pulmonary artery pressure is frequently elevated in patients with post-traumatic pulmonary dysfunction. To ascertain whether or not this increase is reversible and what effects such reversal would have on gas exchange, the vasodilators nitroprusside and nitroglycerine were administered to 11 such patients. Pulmonary hemodynamics an gas exchange were observed. Mean pulmonary artery pressure and pulmonary vascular resistance decreased and pulmonary shunt increased. Cardiac output did not change. These results imply that much of the increase in pulmonary artery pressure is due to a reversible restriction of blood flow past unventilated alveoli. Hypoxic vasoconstriction is postulated to be a major cause of the increase in pulmonary artery pressure.