A reduction of arterial PO2 is generally observed when
vasodilators are given to patients with cardiac or
pulmonary disease. This has been attributed to a release of preexisting hypoxic pulmonary vasoconstriction (HPV). We investigated the effects of hemodynamics and blood
gases of IV
nitroglycerin, IV
nitroprusside and sublingual
nifedipine, at dosages currently used in clinical practice, in 23 healthy volunteers at normoxic conditions (fraction of inspired O2, FIO2 0.21) and at acute inspiratory
hypoxia (FIO2 0.125 during 10 min). Breathing FIO2 0.125 elicited pulmonary vasoconstriction in all the subjects. At FIO2 0.21,
nitroglycerin reduced preload,
nifedipine reduced afterload,
nitroprusside had balanced effects, but none of the drugs induced pulmonary vasodilation and only
nitroglycerin deteriorated arterial oxygenation. At FIO2 0.125,
nitroglycerin did not at all affect the pulmonary pressor response, while both
nitroprusside and
nifedipine decreased it. An inhibition of HPV was obtained with certainty in only one subject who received
nitroprusside. In all the subjects in whom HPV was partially inhibited by
vasodilator administration, the alveolar-arterial PO2 gradients remained significantly lowered, suggesting that the pulmonary vascular tone adaptation to alveolar
hypoxia still was effective in improving ventilation/perfusion relationships. The role of impaired HPV in the reduction of arterial PO2 in patients under
vasodilator therapy may have to be reevaluated.