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The effects of a period of anoxia 18-24 h after birth on bilirubin levels in rat brain were investigated during anoxia, recovery, and development. Postnatal anoxia induces a significant, temporary increase (up to 200% with respect to control values) in newborn rat brain bilirubin levels during anoxia and short-term recovery. Pretreatment of the newborn rats with a single dose of the drug sulfixosazole markedly enhances bilirubin accumulation in the brain of the anoxic rats. A second rise in brain bilirubin concentration is detected in a group of the newborn rats 3-6 days after oxygen deprivation. Autoradiographic localization of radiolabeled bilirubin following in vivo experiments suggests that this substance is preferentially accumulated in some areas of the newborn rat brain as a consequence of postnatal anoxia, and indicates, together with the effect of sulfixosazole, that as a result of anoxia, a displacement of unbound bilirubin from blood to the nervous tissue occurs. Our results confirm the importance of anoxia as a risk factor for the development of bilirubin-induced encephalopathy. The possible relevance of intracerebral hemorrhages caused by perinatal asphyxia producing delayed bilirubin accumulation in the newborn rat brain is suggested.

Effect of Postnatal Anoxia on Bilirubin Levels in Rat Brain