Severe global asphyxia, even if brief, results in prolonged cerebral hypoperfusion in fetal sheep. In this study we sought evidence to support the hypothesis that cerebral hypoperfusion is a consequence of suppressed cerebral metabolism. In the 24 h following complete occlusion of the umbilical cord for 10 min, sagittal sinus blood flow velocity was significantly decreased for up to 12 h. Capillary blood flow, measured using microspheres, decreased at 1 and 5 h after cord occlusion in many brain regions including cortical grey and white matter. Microdialysis probes implanted in the cerebral cortex revealed an increase in extracellular glucose concentrations in grey matter for 7-8 h post-asphyxia, while lactate increased only briefly, suggesting decreased cerebral glucose utilization over this time. While this data, and the concurrent suppression of breathing movements and electrocortical activity supports the concept of hypometabolic hypoperfusion, the significant increase of pyruvate and glycerol concentrations in dialysate fluid obtained from the cerebral cortex at 3-8 h after cord occlusion suggests an eventual loss of membrane integrity, and the prolonged increase of breathing movements for many hours suggests loss of the pontine/thalamic control that produces the distinct pattern of fetal breathing movements, in utero.