HYDRALAZINE DOES NOT INHIBIT CANINE HYPOXIC PULMONARY VASOCONSTRICTION

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Abstract
Clinical experience with hydralazine led to conflicting data concerning its effect on the pulmonary vasculature. The effects of hydralazine were studied on the hypoxic pulmonary vasoconstrictor response in 9 dogs challenged with inhalation of 10% O2 in the presence and absence of hydralazine. Prior to administration of the drug, hypoxia increased cardiac output from 174 .+-. 13 to 209 .+-. 21 ml/kg per min (P < 0.05) and pulmonary artery pressure from 9 .+-. 1 to 19 .+-. 1 mm Hg (P < 0.05). After hydralazine, cardiac output rose during normoxia to 275 .+-. 30 and during hypoxia to 305 .+-. 34 ml/kg per min (P < 0.05). Pulmonary artery pressure continued to respond to hypoxia, rising from 11 .+-. 1 to 21 .+-. 1 mm Hg (P < 0.05) in the presence of hydralazine. Hydralazine reduced pulmonary vascular resistance during normoxia from 173 .+-. 14 to 136 .+-. 13 dyn/s per cm-5 (P < 0.05) but even after the drug, pulmonary vascular resistance rose sharply during hypoxia. There was no significant difference in the response to hypoxia of pulmonary artery pressure or pulmonary vascular resistance after hydralazine when compared with that before hydralazine. In a 2nd set of 6 dogs, these experiments were repeated but the dogs were volume-depleted after the administration of hydralazine to prevent the passive pulmonary vasodilation that occurs because of the rise in cardiac output with the drug. No inhibition of hypoxic pulmonary vasoconstriction by hydralazine was found. Sodium nitroprusside was administered to 4 dogs using the same model and a significant inhibition of hypoxic pulmonary vasoconstriction was found. Hydralazine, unlike nitroprusside, does not inhibit the pulmonary vascular response to hypoxia.