Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport

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Standard

Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport. / Knudsen, G M; Poulsen, H E; Paulson, O B.

In: Journal of Hepatology, Vol. 6, No. 2, 04.1988, p. 187-92.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Knudsen, GM, Poulsen, HE & Paulson, OB 1988, 'Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport', Journal of Hepatology, vol. 6, no. 2, pp. 187-92. https://doi.org/10.1016/s0168-8278(88)80030-8

APA

Knudsen, G. M., Poulsen, H. E., & Paulson, O. B. (1988). Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport. Journal of Hepatology, 6(2), 187-92. https://doi.org/10.1016/s0168-8278(88)80030-8

Vancouver

Knudsen GM, Poulsen HE, Paulson OB. Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport. Journal of Hepatology. 1988 Apr;6(2):187-92. https://doi.org/10.1016/s0168-8278(88)80030-8

Author

Knudsen, G M ; Poulsen, H E ; Paulson, O B. / Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport. In: Journal of Hepatology. 1988 ; Vol. 6, No. 2. pp. 187-92.

Bibtex

@article{e6a8d7f9e66f4cab8e6fca9b5e5c5b88,
title = "Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport",
abstract = "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.",
keywords = "Animals, Blood-Brain Barrier/drug effects, Galactosamine, Hepatic Encephalopathy/chemically induced, Male, Rats, Rats, Inbred Strains, Sodium/pharmacokinetics, Sucrose/pharmacokinetics, gamma-Aminobutyric Acid/pharmacokinetics",
author = "Knudsen, {G M} and Poulsen, {H E} and Paulson, {O B}",
year = "1988",
month = apr,
doi = "10.1016/s0168-8278(88)80030-8",
language = "English",
volume = "6",
pages = "187--92",
journal = "Journal of Hepatology, Supplement",
issn = "0169-5185",
publisher = "Elsevier",
number = "2",

}

RIS

TY - JOUR

T1 - Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport

AU - Knudsen, G M

AU - Poulsen, H E

AU - Paulson, O B

PY - 1988/4

Y1 - 1988/4

N2 - 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.

AB - 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.

KW - Animals

KW - Blood-Brain Barrier/drug effects

KW - Galactosamine

KW - Hepatic Encephalopathy/chemically induced

KW - Male

KW - Rats

KW - Rats, Inbred Strains

KW - Sodium/pharmacokinetics

KW - Sucrose/pharmacokinetics

KW - gamma-Aminobutyric Acid/pharmacokinetics

U2 - 10.1016/s0168-8278(88)80030-8

DO - 10.1016/s0168-8278(88)80030-8

M3 - Journal article

C2 - 3411098

VL - 6

SP - 187

EP - 192

JO - Journal of Hepatology, Supplement

JF - Journal of Hepatology, Supplement

SN - 0169-5185

IS - 2

ER -

ID: 275604855