Cerebral vascular responses to changes in carbon dioxide tension in term and preterm infants with apnea

Carbon dioxide (CO(2)) plays important roles in regulating both respiratory drive and cerebral blood flow. These effects are mediated, in part, by activity of the sympathetic nervous system. We hypothesized that the presence of acute life-threatening events or apnea in term or preterm infants, respectively, would serve as a marker for immaturity of cerebral autonomic innervation and that such infants would display a reduced cerebral vascular response to elevated pCO(2). Therefore, we evaluated the cerebral vascular response during CO(2) challenge tests in groups of term and preterm infants with primary apnea. In term infants (39 +/- 2 weeks gestation) with acute life-threatening events, elevated pCO(2) was accompanied by decreasing pulsatility index and increasing mean anterior cerebral blood flow velocity. However, in preterm infants (29 +/- 2 weeks' gestation) with apnea, pulsatility index and anterior cerebral artery flow velocity did not significantly change in response to CO(2) supplementation. We conclude that preterm, but not term, infants with apnea exhibit impaired vascular responses to hypercarbia.