Nifedipine attenuates acute hypoxic pulmonary vasoconstriction in awake piglets.

The calcium channel blocker nifedipine was administered to awake piglets to determine the drug's potential efficacy as a pulmonary vasodilator in newborns. We hypothesized that nifedipine attenuates acute hypoxic pulmonary vasoconstriction in this age group. Hemodynamic and arterial blood gas measurements were made in 24 catheterized piglets, 10 +/- 3 days of age, while they breathed room air and then 12% O2, 4% CO2, and 86% N2 gas. Thirteen piglets were studied before and after infusions of 15 and 40 micrograms X kg-1 X min-1 of nifedipine prior to hypoxia to see if the drug prevents hypoxic pulmonary vasoconstriction. In 7 animals, nifedipine was administered after the onset of hypoxia to see if the drug reduces ongoing hypoxic pulmonary vasoconstriction. Nifedipine significantly increased heart rate (56 +/- 28%) and cardiac output (48 +/- 45%) and decreased systemic artery pressure (-11 +/- 7%) and systemic vascular resistance (-37 +/- 18%) compared with pretreatment values under normoxic conditions. Pulmonary artery pressure increased (28 +/- 21%) after nifedipine treatment, but total pulmonary resistance remained unchanged during normoxia. Nifedipine did not reduce pulmonary artery pressure compared with pretreatment values during hypoxia, but reduced the elevation in total pulmonary resistance associated with hypoxia by 45 to 99% in a dose-dependent manner. We conclude that nifedipine vasodilates the constricted pulmonary vasculature associated with hypoxia in newborns but that this effect is manifested primarily by a rise in cardiac output rather than by a reduction in pulmonary artery pressure in this age group.