Effect of acute hypoxemia on brain blood flow and oxygen metabolism in immature fetal sheep.

Studies of cerebral blood flow and oxygen metabolism during acute hypoxic hypoxia in fetal sheep have been confined to late gestation, a time when brain development in this species is largely complete. There is no systematic study of cerebral vascular responses to acute hypoxic hypoxia in immature fetal sheep or, indeed, in immature brains of any species. We studied 13 fetal sheep in utero at 93 +/- 1 days gestation (term = 145-150 days), 48 h after intravascular catheters were placed into the superior sagittal sinus, axillary arteries, and inferior vena cava. We measured brain blood flow by the microsphere method. Cerebral oxygen consumption was calculated with the use of blood flow to the cerebral hemispheres (cerebrum, diencephalon, mesencephalon) and arterial and sagittal sinus values for oxygen content. Fractional oxygen extraction was calculated as the ratio between oxygen consumption and oxygen transport. We altered fetal oxygenation by changing the mother's inspired oxygen concentration. As in the near-term fetus, acute hypoxic hypoxia resulted in increased blood flow to cerebral hemispheres, cerebellum, and pons-medulla; furthermore, the increase in blood flow was sufficient to sustain cerebral oxygen consumption. However, in contrast to near-term fetuses, the increase in blood flow to the cerebral hemispheres was not sufficient to maintain convective oxygen transport. Cerebral oxygen consumption was therefore sustained in part by an increase in fractional extraction. Blunted hypoxic vasodilation in immature fetuses might reflect either immature regulatory mechanisms or an inability of cerebral vessels to respond to the usual stimuli. It is also possible that hypoxic vasodilation was blunted by reflex stimulation of the sympathetic nervous system.