Brain Gamma Amino-Butyric Acid in Acute Hepatic Encephalopathy in Dogs Following Hepatectomy with or without Abdominal Evisceration

Pomier‐Layrargues, Gilles; Bories, P; Mirouze, D; Giordan, J; Feneyrou, B; Bellet-Hermann, H.; Marchal, G; Michel, H

doi:10.1007/978-1-4684-4787-3_14

Cited by 3 publications

(1 citation statement)

References 9 publications

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“…The GABA theory states that brain GABA levels are elevated in HE inducing, by a mechanism of upregulation, an increase in the number of specific postsynaptic GABA receptors. Brain GABA levels have not been found to be elevated in rats or dogs with fulminant hepatic failure (22,23) nor in rats with PCS (24). Moreover, GABA levels measured in the brain of cirrhotic patients and patients with fulminant hepatic failure dying in HE were found to be within the normal range (25,26).…”

Section: Controlsmentioning

confidence: 99%

Hepatic encephalopathy in cirrhotic and portacaval shunted dogs: Lack of changes in brain GABA uptake, brain GABA levels, brain glutamic acid decarboxylase activity and brain postsynaptic GABA receptors

et al. 1988

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It has been suggested, from studies of a rabbit model of fulminant hepatic failure, that hepatic encephalopathy might be related to an increase in brain gamma-aminobutyric acid uptake through a more permeable bloodbrain barrier, leading to an overactivity of brain gamma-aminobutyric acid-mediated inhibitory neurotransmission. Five groups of dogs were studied: normal dogs, dogs with secondary biliary cirrhosis without and with hepatic encephalopathy and portacaval shunted dogs without and with hepatic encephalopathy. Brain gamma-aminobutyric acid and sucrose uptake was investigated using the multiple indicator dilution curve technique in unanesthetized dogs. Tracer doses of 99mTc-labeled albumin (extracellular reference substance), 3H-labeled gamma-aminobutyric acid and 14C-labeled sucrose prepared in autologous dog plasma were injected in one carotid artery, and dorsal sagittal sinus dilution curves were obtained. Uptake was calculated by comparing the areas under the 99mTc-labeled albumin and the [3H]gamma-aminobutyric acid (or [14C]sucrose) curves from appearance to peak height. After killing, brain gamma-aminobutyric acid levels were measured in the frontal cortex by high-performance liquid chromatography and glutamic acid decarboxylase activities using a radioenzymatic assay. Brain gamma-aminobutyric acid postsynaptic receptors were assessed using [3H]muscimol binding studies. There were no significant changes in cirrhotic and shunted dogs with or without hepatic encephalopathy with regard to brain gamma-aminobutyric acid and sucrose uptake, brain gamma-aminobutyric acid levels and glutamic acid decarboxylase activities. [3H]Muscimol binding studies did not show any changes in the number nor in the affinity of postsynaptic gamma-aminobutyric acid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Controlsmentioning

confidence: 99%

Hepatic encephalopathy in cirrhotic and portacaval shunted dogs: Lack of changes in brain GABA uptake, brain GABA levels, brain glutamic acid decarboxylase activity and brain postsynaptic GABA receptors

et al. 1988

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Hepatic encephalopathy: Lack of changes of γ-aminobutyric acid content in plasma and cerebrospinal fluid

Moroni¹,

Riggio²,

Carlà³

et al. 1987

Hepatology

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The aim of the study was to verify the role of gamma-aminobutyric acid in the pathogenesis of hepatic encephalopathy occurring in cirrhotic patients by attempting to correlate plasma and cerebrospinal fluid content of authentic gamma-aminobutyric acid with the neurological manifestations of hepatic encephalopathy. For this purpose, plasma and cerebrospinal fluid gamma-aminobutyric acid levels were measured by means of mass fragmentography in 17 cirrhotic patients with hepatic encephalopathy and in 6 cirrhotics without neurological symptoms. Moreover, in all patients, a second sample was obtained during the clinical course of hepatic encephalopathy. The mean plasma and cerebrospinal fluid gamma-aminobutyric acid levels were not different in patients with or without hepatic encephalopathy and did not change during the evolution of the neurological symptoms. The lack of changes in the gamma-aminobutyric acid content in plasma and cerebrospinal fluid during hepatic encephalopathy is in contrast with the hypothesized importance of increased entry into the brain of gamma-aminobutyric acid in the pathogenesis of hepatic encephalopathy.

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Invited Review: Nutritional Support in Hepatic Failure

Hiyama

Fischer

1988

Nut in Clin Prac

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Brain Gamma Amino-Butyric Acid in Acute Hepatic Encephalopathy in Dogs Following Hepatectomy with or without Abdominal Evisceration

Cited by 3 publications

References 9 publications

Hepatic encephalopathy in cirrhotic and portacaval shunted dogs: Lack of changes in brain GABA uptake, brain GABA levels, brain glutamic acid decarboxylase activity and brain postsynaptic GABA receptors

Hepatic encephalopathy in cirrhotic and portacaval shunted dogs: Lack of changes in brain GABA uptake, brain GABA levels, brain glutamic acid decarboxylase activity and brain postsynaptic GABA receptors

Hepatic encephalopathy: Lack of changes of γ-aminobutyric acid content in plasma and cerebrospinal fluid

Invited Review: Nutritional Support in Hepatic Failure

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