Abstract
Five-day-old rats dying during prolonged asphyxia at body temperature (37 C) were found to have a metabolic form of brain damage (increase in brain [ Na +] [ K +] ratio) and brain edema (increase in brain water). Five-day-old rats dying during acute anoxia at body temperature had the same metabolic form of brain damage but not brain edema. Following prolonged asphyxia, metabolic damage was greater in brain stem as compared with forebrain or cerebellum. The presence of brain edema could be related to the severity of brain metabolic damage. During prolonged asphyxia the severity of metabolic brain damage was increased by pretreatment with sodium iodoacetate. Asphyxia at body temperature had a more damaging effect on the brain as compared with asphyxia at room temperature (22–24 C). Asphyxia in the presence of a carbon dioxide absorbant (soda lime) did not alter the severity of metabolic brain damage. It could be speculated that the human neonatal brain may undergo similar changes following birth asphyxia.
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