Pulmonary vascular tone was investigated by the construction of pulmonary arterial pressure (PAP)/cardiac output (&OV0422;) plots, and gas exchange, by the multiple inert gas elimination technique, in 24 anesthetized dogs before and after pulmonary embolization of autologous clots. Three PAP/&OV0422; plots were obtained by a manipulation of venous return at baseline and 60 min and 110 min after embolization. Before the third PAP/&OV0422; plot, the dogs were randomly allocated to one of the following iv treatments: 1) placebo (n = 6); 2) prostaglandin E1(PGE1) 0.4 μg·kg−1·min−1(n = 6); 3) hydralazine 2 mg/kg (n = 6); and 4) nitroprusside 10 μg·kg−1·min−1(n = 6). These vasodilators decreased systemic arterial pressure by a mean of 44%. Ventilation-perfusion (&OV0312;A/&OV0422;) distributions were determined at the same &OV0422; (2.4 ± 0.11·min−1·m−2, mean ± SE) of each PAP/&OV0422; plot. Embolization increased the intercept and the slope of the PAP/&OV0422; plots (p< 0.001). Distributions of &OV0312;A/&OV0422; were only moderately impaired, with an increased dispersion of both &OV0312;Aand &OV0422; and a shift of &OV0312;Adistributions to higher &OV0312;A/&OV0422;. Pao&OV0312;changed from 208 ± 5 to 172 ± 8 mmHg (P< 0.01) (fraction of inspired O20.4). None of the treatments had any effect on &OV0312;A/&OV0422; distributions. Placebo and PGE1had no effect on PAP/&OV0422; plots. Hydralazine and nitroprusside reduced the slope of the PAP/&OV0422; plots. Thus, in this canine model of acute pulmonary embolism: 1) &OV0312;A/&OV0422; distributions were moderately impaired accounting for only slight hypoxemia, and 2) pulmonary hypertension was partially reversible by hydralazine and by nitroprusside without associated non-flow-dependent change in &OV0312;A/&OV0422; distributions and arterial oxygenation.