A neonatal lamb model has been developed to examine the regulation of cerebral blood flow (CBF) and oxygen metabolism during the critical period after an asphyxial insult. Nine newborn lambs had control measurements and timed measurements after asphyxia of CBF (radioactive microsphere technique), arterial and cerebral venous (sagittal sinus) blood gases and oxygen contents performed. Immediately after resuscitation from asphyxia, there was a marked increase in CBF compared to control (239 +/- 22 versus 82 +/- 7 ml X 100 g-1 X min-1, mean +/- SEM; p less than 0.01). Cerebral oxygen delivery (CBF X arterial O2 content) increased from 12.87 +/- 1.20 to 37.40 +/- 3.40 ml X 100 g-1 X min-1 (p less than 0.01), while cerebral O2 consumption was significantly decreased compared to control (4.75 +/- 0.42 to 3.42 +/- 0.46 ml X 100 g-1 X min-1, p less than 0.05). Cerebral fractional O2 extraction, the relationship between oxygen uptake and delivery fell from 0.38 +/- 0.03 to 0.09 +/- 0.02; p less than 0.01. This reactive hyperemia was followed in all animals by a period of hypoperfusion. CBF (52 +/- 4 ml X 100 g-1 X min-1), O2 delivery (7.94 +/- 0.50 ml X 100 g-1 X min-1), and cerebral O2 consumption (3.34 +/- 0.24 ml X 100 g-1 X min-1) were all significantly depressed when compared to control. These data demonstrate important changes in CBF and O2 metabolism after neonatal asphyxia that may be important to the pathogenesis of brain injury.