We studied the effects of prolonged (6 hours) hypocapnia and the abrupt termination thereof on cerebral blood flow and metabolism in six paralyzed, sedated (but not anesthetized) newborn lambs. Thirty minutes after institution of hyperventilation to an arterial carbon dioxide pressure of 15 +/- 2 torr, hyperventilation, cerebral blood flow had returned to baseline. Abrupt termination of hyperventilation after 6 hours resulted in a 110 +/- 71% increase in cerebral blood flow over baseline after 30 minutes of normocapnia. This cerebral hyperemia persisted for at least 90 minutes after hyperventilation was discontinued. Cerebral oxygen consumption did not change throughout the study. The posthypocapnia hyperemia noted in these animals after abrupt normalization of arterial carbon dioxide pressure may contribute to the increased risk of intracranial hemorrhage in newborn infants who are treated similarly in the management of pulmonary hypertension.