The quantitative autoradiographic [14C]iodoantipyrine technique was applied to measure the effects of an acute hypoxic exposure on rates of local cerebral blood flow (LCBF) in the 10 (P10)-, 14 (P14)- and 21 (P21)-day-old rat. The animals were exposed to hypoxic (7% O2/93% N2) or control gas mixtures (21% O2/79% N2) for 40 min before the initiation of the 1-min LCBF measurement. At P10, hypoxia induced a 142-415% increase in LCBF over control levels, which affected the 45 structures studied. The highest increases in LCBF were noticed in posterior midbrain and brainstem regions. These increases are in good accordance with hypoxia-induced increases in LCBF recorded during acute hypoxia exposure in both newborn and adult animals. At P14 and P21, rates of LCBF decreased with hypoxia. These decreases were significant in 23 and 21 brain regions, respectively, belonging to all systems studied. These changes in LCBF are in quite good correlation with our previous data on the effects of acute hypoxia exposure on cerebral glucose utilization but the decrease in LCBF is of higher amplitude than the one in cerebral glucose utilization translating into a relative hypoperfusion at a constant metabolic level at P14 and P21. However, arterial blood pressure was reduced by 16 mmHg and arterial pCO2 was significantly decreased at the two latter ages in hypoxic animals compared to controls. These two systemic factors, and mainly hypocapnia, are rather responsible for the cerebral hypoperfusion recorded at P14 and P21 in hypoxic rats whereas the circulatory response seems to be predominantly hypoxic at P10.