Role of the cerebrovascular and metabolic responses in the delayed phases of injury after transient cerebral ischemia in fetal sheep

Background and Purpose-Perinatal hypoxic-ischemic injuries can trigger a ca scade of events leading to delayed deterioration and cell death several hou rs later. The objective of this study was to characterize the cerebral bloo d flow responses and the changes in extracellular glucose and lactate durin g the delayed phases of injury and to determine their relationships with th e pathophysiological events after hypoxic-ischemic injury. Methods-Two groups of near-term chronically instrumented fetal sheep were s ubjected to 30 minutes of cerebral hypoperfusion. In the first group, regio nal cerebral blood flow was measured over the next 24 hours with radiolabel ed microspheres, In the second, cortical extracellular glucose and lactate were measured by microdialysis. Parietal electrocorticographic activity and cortical impedance were recorded continuously in both groups, and the exte nt of neuronal loss was determined histologically at 72 hours after injury, Results-Cerebral blood flow was transiently impaired in the cortex during r eperfusion, whereas during the delayed phase, there was a marked increase i n cerebral blood flow. The severity of cortical neuronal loss was related t o the degree of hypoperfusion in the immediate reperfusion period and inver sely related to the magnitude of the delayed hyperperfusion. Cortical extra cellular lactate was elevated after injury, and both glucose and lactate se condarily increased during the delayed phase of injury. Conclusions-The delayed phase is accompanied by a period of hyperperfusion that may protect marginally viable tissue.