To study the delivery of oxygen to the cerebral tissue during metabolic acidosis and its therapy with bicarbonate (NaHCO3), oxygen partial pressure of the cisternal fluid was measured in 12 experiments of HCl-induced acidemia and eight experiments of diabetic ketoacidosis in 16 unanesthetized dogs. Full correction of acidosis with bicarbonate caused a significant (P less than 0.05) decrease in Pcsf 2: in the HCl acidotic dogs, Pcsfo2 decreased from 53.9 +/- 2.2 torr to 45.9 +/- 2.3 torr within one hour; in the ketoacidotic dogs, Pcsfo2 decreased for 48.5 +/- 5.4 torr to 26.7 +/- 6.6 torr within six hours. In the ketoacidotic dogs not treated with bicarbonate, there was no significant change in Pcsfo2. An inverse relationship (P less than 0.01) between the cisternal lactic acid level and the cisternal PO2 was also observed. It is concluded that NaHCO3 therapy in diabetic ketoacidosis decreases the cerebral O2 availability and that cerebral hypoxia contributes to the brain dysfunction encountered after the initiation of such therapy in acidemia.