METABOLIC RESPONSES OF THE NEONATAL RABBIT BRAIN TO HYDROCEPHALUS ANDSHUNTING

The metabolic changes that occur in the neonatal brain as a result of hydrocephalus, and the response to ventriculoperitoneal shunting, vary with the maturational stage of the brain. In this study, local glucos e utilization (LCMRS(glu)) and oxidative metabolic capacity were estim ated using 2-deoxyglucose autoradiography and cytochrome oxidase histo chemistry, respectively. Hydrocephalus was induced in rabbit pups via intracisternal kaolin injections at 4-6 days of age. Shunting occurred at 19-26 days of age and the animals were sacrificed at ages ranging from 33 to 331 days. In normal animals there was a high glucose demand early in life which showed a decrease at about 60 days of age. In rab bits sacrificed prior to 60 days of age the controls showed the highes t LCMR(glu) with significant decreases in both the hydrocephalic and s hunted animals. After 60 days of age the shunted animals had higher LC MR(glu), than both the hydrocephalic and control subjects. Oxidative m etabolic capacity peaked before 50 days of age in normal animals. At t he youngest age, both the hydrocephalic and shunted animals showed hig her cytochrome oxidase density rates than the control rabbits. In the older group, the hydrocephalic animals remained high while the shunted animals approximated the control densities. Neither the changes seen in the LCMR(glu) nor the oxidative metabolic capacity were correlated with changes in cell packing density or increased intracranial pressur e. These data suggest that when the brain is compromised by hydrocepha lus, there is an initial compensatory increase in oxidative metabolic capacity. The development of the glycolytic pathway appears to be reta rded by hydrocephalus, but with shunting and the passage of time,the L CMR(glu) rebounds to levels above that of controls.