Electron microscopic study of the brain edema in D-galactosamine induced acute liver failure of rats.

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Brain tissue in the acute liver failure induced in rats with D(+)-galactosamine hydrochloride (GalN, 2.5g/kg BW, ip), was examined electron microscopically. 56-72 hours after the ad-ministration of GalN when hepatic coma developed in association with massive hepatic necrosis, the brain water contents was increased mainly in the brain stem and the cerebellum. Under microscopic observation, brain tissue was characterized by intracellular edema such as marked hydropic swelling of the foot processes of the astrocyte with changes of mitochondria. Howeverneither the disruption of the tight junction of the capillary endothelium nor enlargement of the extracellular space was noted in this model. In the rats injected with horseradish peroxidase (HRP) from the peripheral vein, the number of HRP-containing vesicles was slightly increased in the capillary endothelium, but lanthanum nitrate injected via the aorta remained within the capillary lumen. It was suggested that increased amount of toxic agents may lead to the intracellular edema in the brain without marked changes of the capillary such as disruption of the tight junction in D(+)-galactosamine induced acute liver failure model.
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