Progressive changes in cortical water and electrolyte content at three stages of rat infantile hydrocephalus and the effect of shunt treatment.

Infantile hydrocephalus causes injury to the developing brain and despite surgical treatment, neurological deficits persist. The H-Tx rat develops inherited hydrocephalus in late gestation. Rapid postnatal ventricular enlargement, results in severe hydrocephalus by 21 days after birth. This is accompanied by changes in cortical morphology and metabolite content that indicate possible changes in intracellular composition. This study has tested the hypothesis that tissue water and electrolyte content is altered in hydrocephalus. The objective was to gain further insight into the mechanisms leading to neuronal damage. Water and electrolyte content (Na+, Cl-, and K+) were measured in the cerebral cortex of control and hydrocephalic rats at 4, 11, and 21 days after birth, and at 21 days in rats that received alleviating shunt surgery at 4 or 11 days. At all ages, hydrocephalic tissue was significantly increased over control for cortical water, Na+, and Cl- content. Additionally, at the intermediate (11-day) and advanced (21-day) stages there were significant decreases in K+ content, consistent with previous observations of decreases in organic osmolytes and energy metabolites. This suggests that by 11 days there are intracellular changes, probably through impaired membrane homeostatic mechanisms. In shunt-treated rats, the extracellular constituents were almost normal, although a small increase over control values persisted. The decrease in intracellular K+ was not corrected in either group of shunt-treated rats. It is concluded that early hydrocephalus is characterized by extracellular edema that largely reverses with shunt treatment. Subsequently, as the hydrocephalus progresses, there is a breakdown of cell homeostasis and an irreversible loss of intracellular constituents.