Cerebral hypoxia‐ischemia remains a major cause of acute perinatal brain injury. Research in experimental animals over the past decade has greatly expanded our knowledge of those oxidative events which occur during a hypoxic‐ischemic insult to the brain, as well as those metabolic alterations which evolve during the recovery period following resuscitation. The available evidence suggests that hypoxia alone does not lead to brain damage, but rather a combination of hypoxia‐ischemia or isolated cerebral ischemia is a necessary prerequisite for tissue injury to occur. Furthermore, hypoxia‐ischemia severe enough to produce irreversible tissue injury is always associated with major perturbations in the energy status of the perinatal brain which persists well into the recovery period. The lingering energy depletion sets in motion a cascade of biochemical alterations that are initiated during the course of the insult and proceed well into the recovery period to culminate in either neuronal necrosis or infarction. Unlike the adult, where glucose supplementation prior to or during hypoxia‐ischemia accentuates tissue injury, glucose treatment of perinatal animals subjected to a similar insult substantially reduces the extent of tissue injury. The mechanism for the age‐specific effect of glucose on hypoxic‐ischemic brain damage is discussed in relation to pathogenetic mechanisms responsible for the occurrence of permanent
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