EFFECT OF DOPAMINE ON HYPOXIC VENTILATORY RESPONSE OF SEDATED PIGLETSWITH INTACT AND DENERVATED CAROTID-BODIES

To determine whether the neonatal hypoxic ventilatory depression is in part produced by an increased endogenous dopamine release that can de press the activity of central and peripheral chemoreceptors, 31 sedate d and spontaneously breathing newborn piglets [age 5 +/- 1 (SD) days; weight 1.7 +/- 0.4 kg] were randomly assigned to an intact carotid bod y or a chemodenervated group. Minute ventilation (VE), arterial blood pressure, and cardiac output (CO) were measured in room air before inf usion of saline or the dopamine antagonist flupentixol (0.2 mg/kg iv) and 15 min after drug infusion and were repeated after 10 min of hypox ia (inspiratory O-2 fraction = 0.10). VE increased significantly after 10 min of hypoxia in the piglets that received flupentixol independen t of whether the carotid bodies were intact or denervated. However, th e increase in VE was largest and sustained throughout the 10 min of hy poxia only in the intact carotid body flupentixol group. As expected, the initial increase in VE with hypoxia was abolished by carotid body denervation. Changes in arterial blood gases, CO, and mean arterial bl ood pressure with hypoxia were not different among groups. These resul ts demonstrate that flupentixol reverses the late hypoxic decrease in VE, acting through peripheral and central dopamine receptors. This eff ect is not related to changes in cardiovascular function or acid-base status.