EFFECTS OF VASODILATORS ON GAS-EXCHANGE IN ACUTE CANINE EMBOLIC PULMONARY-HYPERTENSION

Pulmonary vascular tone was investigated by the construction of pulmonary arterial pressure (PAP)/cardiac ouput (Q̇) 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/Q̇ plots were obtained by a manipulation of venous return at baseline and 60 min and 110 min after embolization. Before the third PAP/Q̇ 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 (V̇(A)/Q̇) distributions were determined at the same Q̇ (2.4 ± 0.1 l · min-1 · m-2, mean ± SE) of each PAP/Q̇ plot. Embolization increased the intercept and the slope of the PAP/Q̇ plot (P < 0.001). Distributions of V̇(A)/Q̇ were only moderately impaired, with an increased dispersion of both V̇(A) and Q̇ and a shift of V̇(A) distributions to higher V̇(A)/Q̇. Pa(O2) changed from 208 ± 5 to 172 ± 8 mmHg (P < 0.01) (fraction of inspired O2 was 0.4). None of the treatments had any effect on V̇(A)/Q̇ distributions. Placebo and PGE1 had no effect on PAP/Q̇ plots. Hydralazine and nitroprusside reduced the slope of the PAP/Q̇ plots. Thus, in this canine model of acute pulmonary embolism: 1) V̇(A)/Q̇ 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 V̇(A)/Q̇ distributions and arterial oxygenation.