CEREBRAL METABOLIC CONSEQUENCES OF NEONATAL PATHOLOGIES IN THE IMMATURE RAT

The cerebral metabolic consequences of hypoxia, seizures and hyperbili rubinemia were explored in immature rats between the postnatal age of 10 (P10) and 21 days (P21) by the quantitative autoradiographic [C-14] 2-deoxyglucose technique. The effects of a previous bilirubin exposure on cerebral regional permeability to bilirubin were measured by autor adiography. Hypoxia was induced by breathing a 7% N-2/93% O-2 gas mixt ure and seizures were initiated by injections of pentylenetetrazol. Hy perbilirubinemia was induced by the perfusion of a bilirubin/albumin s olution. Hypoxia and seizures induced a general increase in cerebral m etabolic rates to glucose (LCMRglc) in P10 rats, except in hippocampus during seizures. At P14, LCMRglc remained increased during seizures, except in the hippocampus. During hypoxia, LCMRglc were unchanged in t he genu of the corpus callosum and the anterior commissure and decreas ed in the cerebellar white matter. At P21, LCMRglc decreased in all wh ite matter regions during hypoxia and in the hippocampus during seizur es, while they were unchanged in the amygdala and increased in the nuc leus of the solitary tract. During hyperbilirubinemia, LCMRglc decreas ed at all ages with very marked changes in the nucleus of the auditory nerve at P10 and in the inferior colliculus at P21 (72-86%). Twofold decreases were also recorded in the hippocampus. The basic regional ce rebral permeability to the anion was higher at P10 than at P21 and the marked increases in regional permeability to bilirubin after a previo us exposure to the anion were located in the nucleus of the auditory n erve and the hippocampus.