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.