[Effects of hydralazine in hypoxic vasoconstriction. Its study in a canine model of lobar atelectasis]

To determine whether hydralazine (H) a systemic vasodilator, inhibits hypoxic pulmonary vasoconstriction (HPV) we studied in a canine model of lobar atelectasis (LA) the circulatory changes during the following interventions: a) control 1 (LA = HPV), b) during the acute effect produced by opening bilateral arteriovenous fistulas (OF), c) after the closure of the fistulas (CF) (control 2), d) after infusing H (0.33 mg/kg) and e) bleeding the animal at the end of the experiment (control 3). Once HPV was stabilized (control 1), both opening the fistulas and infusing H produced a similar and significant increase in cardiac output and a decrease in resistance (p less than 0.05). Mixed venous oxygen tension (PvO2) closely followed the changes in cardiac output (Qt). Intrapulmonary shunt (Qs/Qt) significantly increased (p less than 0.05) with the fistulas open and with H infusion. CF and bleeding the animal at the end of the experiment reversed the changes in Qt and Qs/Qt. The similar increases in Qt and Qs/Qt by OF or infusing H seems to be related to the levels of pVO2. Our data suggest that hydralazine inhibits pulmonary vasoconstriction probably by raising the level of pVO2 although a direct pulmonary vasodilatory effect of the drug could not be ruled out.