['Local formation of nitric oxide in the lung induces vasodilation in proportion to ventilation and is a putative mechanism behind ventilation-perfusion matching. We hypothesized that regional ventilation-perfusion matching occurs in part due to local constitutive nitric oxide formation.', 'Ventilation and perfusion were analyzed in lung regions (≈1.5 cm) before and after inhibition of constitutive nitric oxide synthase with N-nitro-L-arginine methyl ester (L-NAME) (25 mg/kg) in 7 prone sheep ventilated with 10 cm H2O positive end-expiratory pressure. Ventilation and perfusion were measured by the use of aerosolized fluorescent and infused radiolabeled microspheres, respectively. The animals were exsanguinated while deeply anesthetized; then, lungs were excised, dried at total lung capacity, and divided into cube units. The spatial location for each cube was tracked and fluorescence and radioactivity per unit weight determined.', 'After administration of L-NAME, pulmonary artery pressure increased from a mean of 16.6-23.6 mm Hg, P = .007 but PaO2, PaCO2, and SD log(V/Q) did not change. Distribution of ventilation was not influenced by L-NAME, but a small redistribution of perfusion from ventral to dorsal lung regions was observed. Perfusion to regions with the highest ventilation (fifth quintile of the ventilation distribution) remained unchanged after L-NAME.'] Does inhibition of Constitutive Nitric Oxide Synthase Influence Ventilation-Perfusion Matching in Normal Prone Adult Sheep With Mechanical Ventilation?