Acute respiratory distress syndrome continues to be associated with significant morbidity and mortality related to ventilation-perfusion mismatch,
pulmonary hypertension, and right ventricular failure. It has been suggested that inhaled
nitric oxide, which is a selective pulmonary
vasodilator, may be effective in the treatment of
acute respiratory distress syndrome; however, the effects of
nitric oxide on cardiopulmonary interactions are poorly understood. We therefore developed a model of
acute lung injury that mimics the clinical syndrome of
acute respiratory distress syndrome. In our model, inhaled
nitric oxide significantly reduced pulmonary artery pressure, pulmonary vascular resistance, and pulmonary vascular impedance. In addition, inhaled
nitric oxide improved transpulmonary vascular efficiency and ventilation-perfusion matching, which resulted in increased arterial
oxygen tension. Although arterial
oxygen tension increased,
oxygen delivery did not improve significantly. These data suggest that by improving ventilation-perfusion matching and arterial
oxygen tension while lowering pulmonary vascular resistance and impedance,
nitric oxide may be beneficial in patients with
acute respiratory distress syndrome. However, additional measures to enhance cardiac performance may be required.