Effect of postnatal anoxia on bilirubin levels in rat brain.

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.