The effects of galactosamine-induced hepatic failure upon blood-brain barrier permeability.
The role of changes in blood-brain barrier permeability in the pathogenesis of hepatic encephalopathy remains uncertain. To test the hypothesis that brain microvessel permeability is nonselectively increased in hepatic encephalopathy we measured the blood-brain barrier permeability-surface area product in rats with acute liver failure induced by intraperitoneal injection of galactosamine. The permeability-surface area products to the diffusion-limited tracers, sucrose and methylaminoisobutyric acid, were determined as a measure of blood-brain barrier permeability. Animals were examined 24, 36 and 42 hr after injection, at times when they were stuporous, but not comatose. No significant elevations of the permeability-surface area products for either compound were detected in clinically affected experimental animals when compared to controls. Our results indicate there is no generalized increase in brain vascular permeability during hepatic insufficiency in precomatose animals.
D000818:Animals; D001812:Blood-Brain Barrier; D056486:Chemical and Drug Induced Liver Injury; D005688:Galactosamine; D006501:Hepatic Encephalopathy / Q000209:etiology; D008099:Liver / Q000201:enzymology; D008107:Liver Diseases / Q000201:enzymology / Q000503:physiopathology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D000637:Transaminases / Q000097:blood
D005688:Galactosamine; D000637:Transaminases