Our earlier studies showed no secondary postischemic (PI) rise in cisterna magna pressure (CMP) for ten hours and no significant reduction in CBF (integrated N2O desaturation technique) for three and one-half hours after 15 minutes of systemic circulatory arrest. However, transtentorial pressure gradients may have developed, and CBF changes may have been masked by limitations of the N2O method in low flow states. In this study, 12 dogs were subjected to 15 minutes of aortic occlusion and studied for two hours PI. Immediately after restoration of circulation, cisterna magna, supracortical and lateral ventricle pressures rose to 35 to 40 torr, concomitant with a threefold increase in cerebral blood flow (133Xe clearance technique). By 30 minutes postischemia, cisterna magna and supracortical pressures had returned to control values but lateral ventricular pressures normalized slower. CBF decreased to and remained at 50% of preischemic values after 40 minutes PI. Cerebral glucose uptake increased markedly immediately PI, then fell significantly below control values at 45 minutes. Cerebral O2uptake was significantly reduced, although less than for glucose, between 30 and 60 minutes PI. Global ischemia for 15 minutes is followed neither by a secondary rise in intracranial pressure nor by a cerebrospinal fluid pressure gradient but rather by hypoperfusion and defective glucose metabolism.