In anesthetized normocapnic and normotensive dogs, the effect of arterial hypoxemia on cerebral blood flow and oxidative carbohydrate metabolism was studied. The results are as follows: 1) The hypoxic vasodilatory effect on cerevral vessels is intact even at profound systemic hypoxemia(Pao2 30 torr) if Paco2 is controlled within normal limits. 2) CMRO2 did not significantly increase above the normal even during profound arterial hopoxemis, indicating that CMRO2 levels are poor indices of hypoxia. 3) A disporportinately high glycolysis at Pao2 of 50 torr suggested early cerebral metabolic changes which became more marked with further decrease in Pao2. 4) One hour after restitution of normoxia, however, carebral blood flow and metabolism manifested complete recovery. 6) It is concluded that a transient(20 minutes) profoun systemic arterial hypoxemia does not produce prolonged disorder of cerebral blood flow and oxidative carbohydrate metabolism provided that the cerebral perfusion pressure is kept normal.