Significant discrepancy exists between radioreceptor and high-performance liquid chromatographic estimates of plasma GABA concentrations in animal models of hepatic encephalopathy. A possible explanation for this discrepancy is the presence in plasma of a substance that can inhibit PHI-GABA binding
Plasma gaba, gaba-like activity and the brain gaba-benzodiazepine receptor complex in rats with chronic hepatic encephalopathy
โ Scribed by Jill E. Maddison; Peter R. Dodd; Murray Morrison; Graham A. R. Johnston; Geoffrey C. Farrell
- Publisher
- John Wiley and Sons
- Year
- 1987
- Tongue
- English
- Weight
- 983 KB
- Volume
- 7
- Category
- Article
- ISSN
- 0270-9139
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โฆ Synopsis
Plasma 7-aminobutyric acid (GABA)-like activity, plasma GABA and the brain GABA-benzodiazepine receptor wmplex were studied in rats with chronic hepatic encephalopathy. Portal vein ligation (after prior subcutaneoas transposition of the spleen) results in complete portal bypass of splanchnic blood. In addition, significant hepatocellular damage was superimposed on this model of portosystemic shunting by ligation of the common bile duct. Plasma GABA-like activity (determined by radioreceptor assay) and true plasma GABA concentrations (determined by high-performance liquid chromatography) were found to be significantly increased in both portal vein-ligated and portal vein and bile duct-ligated rats, compared with controls. However, plasma GABA-like activity was consistently greater than the concentration of true GABA in the plasma of all rats. This suggested the presence of a GABA-like faator in plasma that can inhibit ['HIGABA binding, but is not GABA itself. The concentration of this GABA-like faetor was significantly increased in the plasma of rats with chronic hepatic encephalopathy.
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