The effects of intravenous ketamine (1 mg/kg) on cerebral cortical blood flow and O2 uptake were evaluated in 13 anesthetized, ventilated rabbits. Blood flow was measured either directly (Group 1) or by the H2 clearance method (Group 2). In those animals of Groups 1 and 2 with normal control arterial pH (pHa), ketamine produced a significant increase in cerebral cortical blood flow of 18 and 34%, respectively, but had no effect on cerebral cortical O2 uptake. However, in rabbits with low control pHa, ketamine caused an increase in blood flow (30%) accompanied by a significant increase in O2 uptake (22%). Ketamine produced nonsignificant changes in mean arterial blood pressure and arterial blood gases, except for a significant reduction in pressure in animals with low pHa. It is concluded that ketamine is a cerebral vasodilator without cerebral metabolic effect when mean arterial blood pressure and arterial PCO2, PO2, and pH are held constant at physiologic levels. The vasodilator effect of ketamine is probably due to direct dilating action or activation of a cholinergic cerebral vasodilator system.