"Closing volume" (CV) was measured in 18 anaesthetized dogs before, during and after pulmonary vascular congestion produced by inflation of a balloon placed in the left atrium. In group A 10 dogs were anaesthetized with pentobarbitone. CV increased from 30.0 +/- 1.2 to 42 +/- 5.6% of vital capacity (P less than 0.05) when pulmonary wedge pressure was increased from 0.21 +/- 0.27 to 1.54 +/- 0.44 kPa (1.6 +/- 2.0 to 11.6 +/- 3.3 mm Hg) (P less than 0.05). In seven of these 10 dogs gas exchange was impaired after an increase of left atrial pressure. These changes in lung function during pulmonary vascular congestion were not associated with an increase in lung water. In group B, eight dogs were studied after anaesthesia with chloralose and urethane. Vagotomy or vagal cooling to 0 degrees C returned CV to baseline values in six dogs with pulmonary vascular congestion. In two dogs in which bilateral vagotomy had been performed before pulmonary vascular congestion there was no change in CV after balloon inflation. Isoprenaline abolished the effect of pulmonary vascular congestion on closing volume. This suggests that the vagus mediates the changes in lung mechanics associated with pulmonary vascular congestion.