Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport
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Blood-brain barrier permeability to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), to sucrose and to sodium was studied in rats with galactosamine-induced liver damage and hepatic encephalopathy by means of an arterial integral uptake technique. Permeability to GABA was unaltered in all examined brain regions (2.47 +/- 0.25.10(-5) cm3.s-1.g-1, mean +/- S.D.) as compared to control rats (2.49 +/- 0.19.10(-5) cm3.s-1.g-1). The permeability to sucrose (galactosamine 0.25 +/- 0.02 vs. controls 0.24 +/- 0.02.10(-5) cm3.s-1.g-1) and to sodium (galactosamine 5.33 +/- 0.04 vs. controls 5.40 +/- 0.05.10(-5) cm3.s-1.g-1) was also unchanged in hepatic encephalopathy. At the time of investigation mean liver function measured by antipyrine clearance was reduced from 0.39 in control rats to 0.23 ml/min/100 g body wt. in galactosamine-treated animals. The present study does not support the suggestion that peripheral GABA penetrates the blood-brain barrier to any higher extent in hepatic encephalopathy. This provides evidence against at least part of the GABA-hypothesis. Furthermore, an unspecific increased blood-brain barrier permeability in hepatic encephalopathy, as measured by sucrose and sodium uptake, was not found. It is concluded that the GABA-theory requires further careful reevaluation.
Original language | English |
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Journal | Journal of Hepatology |
Volume | 6 |
Issue number | 2 |
Pages (from-to) | 187-92 |
Number of pages | 6 |
ISSN | 0168-8278 |
DOIs | |
Publication status | Published - Apr 1988 |
- Animals, Blood-Brain Barrier/drug effects, Galactosamine, Hepatic Encephalopathy/chemically induced, Male, Rats, Rats, Inbred Strains, Sodium/pharmacokinetics, Sucrose/pharmacokinetics, gamma-Aminobutyric Acid/pharmacokinetics
Research areas
ID: 275604855