Brain edema and intracranial hypertension in rats after total hepatectomy.

BACKGROUND/AIMS: Glutamine, generated from ammonia in astrocytes, may account for brain edema in acute liver failure. Recent studies showing decreased intracranial pressure after hepatectomy in humans suggest that factors released by the necrotic liver could play a pathogenic role in brain swelling. The aim of this study was to examine whether brain edema and intracranial hypertension develop in hepatectomized rats.
METHODS: Rats underwent a portacaval anastomosis or a sham operation. At 24 hours, animals underwent a second sham operation or a total hepatectomy. Intracranial pressure was continuously monitored, and cortical water and glutamine contents were measured after the rats were killed. In a second experiment, hepatectomized and devascularized (portacaval anastomosis plus hepatic artery ligation) rats were killed every 2 hours and at the time of intracranial hypertension.
RESULTS: Although brain edema developed in both groups with liver failure, devascularization resulted in a higher brain water content in spite of an equivalent increase in glutamine concentration. Intracranial pressure increased to a similar degree in both groups, but all parameters increased earlier in anhepatic rats.
CONCLUSIONS: Hepatectomized rats develop brain edema and intracranial hypertension. The temporal sequence in this model supports the role of glutamine as an organic osmolyte. In addition, other factors (e.g., brain volume) may contribute to intracranial hypertension in hepatectomized rats.