Changes in cerebral blood flow, cerebral metabolites, and breathing movements in the sheep fetus following asphyxia produced by occlusion of the umbilical cord.

Severe global fetal asphyxia, if caused by a brief occlusion of the umbilical cord, 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 gray and white matter. Microdialysis probes implanted in the cerebral cortex revealed an increase in extracellular glucose concentrations in gray matter for 7-8 h postasphyxia, while lactate increased only briefly, suggesting decreased cerebral glucose utilization over this time. Although these data, as well as the concurrent suppression of breathing movements and electrocortical activity, support 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. 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.