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Dexamethasone Prevents Hypoxia/Ischemia‐Induced Reductions in Cerebral Glucose Utilization and High‐Energy Phosphate Metabolites in Immature Brain

Abstract: We examined the potential importance of dexamethasone‐mediated alterations in energy metabolism in providing protection against hypoxic‐ischemic brain damage in immature rats. Seven‐day‐old rats (n = 165) that had been treated with dexamethasone (0.1 mg/kg, i.p.) or vehicle were assigned to control or hypoxic‐ischemic groups (unilateral carotid artery occlusion plus 2–3 h of 8% oxygen at normothermia). The systemic availability of alternate fuels such as β‐hydroxybutyrate, lactate, pyruvate, and free fatty acids was not altered by dexamethasone treatment, and, except for glucose, brain levels were also unaffected. At the end of hypoxia, levels of cerebral high‐energy phosphates (ATP and phosphocreatine) were decreased in vehicle‐ but relatively preserved in dexamethasone‐treated animals. The local cerebral metabolic rate of glucose utilization (lCMRgl) was decreased modestly under control conditions in dexamethasone‐treated animals, whereas cerebral energy use measured in a model of decapitation ischemia did not differ significantly between groups. The lCMRgl increased markedly during hypoxia‐ischemia (p < 0.05) and remained elevated throughout ischemia in dexamethasone‐but not vehicle‐treated groups, indicating an enhanced glycolytic flux with dexamethasone treatment. Thus, dexamethasone likely provides protection against hypoxic‐ischemic damage in immature rats by preserving cerebral ATP secondary to a maintenance of glycolytic flux.