[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.
D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D006830:Hydralazine / Q000627:therapeutic use*; D000860:Hypoxia / Q000188:drug therapy*; D008297:Male; D010100:Oxygen / Q000097:blood; D001261:Pulmonary Atelectasis / Q000188:drug therapy / Q000503:physiopathology*; D011652:Pulmonary Circulation; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects*
D006830:Hydralazine; D010100:Oxygen
Efecto de la hidralazina en la vasoconstricción hipóxica. Su estudio en un modelo canino de atelectasia lobar.