Monitoring of Neurotransmitter Amino Acids by Means of An Indwelling Cisterna Magna Catheter: A Comparison of Two Rodent Models of Fulminant Liver Failure

Swain, Margaret S.; Bergeron, Marcelle; Audet, Robert M.; Blei, Andrés T.; Butterworth, Roger F.

doi:10.1002/hep.1840160428

Cited by 74 publications

(51 citation statements)

References 20 publications

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“…The increase in extracellular concentrations of the above-mentioned amino acids in hyperammonaemia-induced encephalopathy is in agreement with other experimental studies who studied (sub)acute encephalopathy (40)(41)(42)(43). However, Rao et al (44) did not find similar increases.…”

Section: Ad 2 Higher Concentrations Of Csf Glutarnine Glutamate Assupporting

confidence: 90%

The effects of ammonia and portal-systemic shunting on brain metabolism, neurotransmission and intracranial hypertension in hyperammonaemia-induced encephalopathy

Vogels¹,

Steynen²,

Maas³

et al. 1997

Journal of Hepatology

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The effects of ammonia and portal-systemic shunting on brain metabolims, neurotransmission and intracranial hypertension in hyperammonaemia-induced encephalopathy Vogels, B.A.P.M.; van Steynen, B.; Maas, M.A.W.; Jorning, G.G.A.; Chamuleau, R.A.F.M. General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Background/Aims: The pathogenetic factors contributing to encephalopathy in portacaval shunted rats with hyperammonaemia were studied. Methods: Hyperammonaemia was induced by ammonium-acetate infusions in portacaval shunted rats (2.8 mmol-kg bw-'*h-l; AI-portacaval shunted rats) and in sham-portacaval shunted rats (6.5 mmol-kg bw-l-h-'; AI-NORM rats). Severity of encephalopathy was quantified by clinical grading and EEG spectral analysis. Changes in brain metabolites were assessed by amino acid analysis of brain cortex homogenates, whereas changes in amino acids with neurotransmitter activity were assessed in cerebrospinal fluid; brain water content was measured by subtracting dry from wet brain weights and intracranial pressure was measured by a pressure transducer connected to a cisterna magna cannula. Results:Although similar increased blood and brain ammonia concentrations were obtained in both experimental groups, only AI-portacaval shunted rats developed encephalopathy, associated with a significant increase in intracranial pressure. HEPATIC encephalopathy (HE) is generally regarded to be a reversible neuropsychiatric syndrome in patients with liver failure. It is often associated with portal-systemic shunting of blood, which may occur spontaneously or be surgically induced. Although the pathogenesis of HE is probably multi- Conclusions: These results indicate that hyperammonaemia alone does not induce encephalopathy, whereas portal-systemic shunting adds an essential contribution to the pathogenesis of encephalopathy. It is hypothesised that the larger increase in brain glutamine in AI-portacaval shunted rats than in AI-NORM rats is responsible for increased brain concentrations of aromatic amino acids, for cell swelling and for extracellular release of glutamate and aspartate. This might promote encephalopathy. If cell swelling is not restricted, intracranial hypertension will develop

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Section: Ad 2 Higher Concentrations Of Csf Glutarnine Glutamate Assupporting

confidence: 90%

The effects of ammonia and portal-systemic shunting on brain metabolism, neurotransmission and intracranial hypertension in hyperammonaemia-induced encephalopathy

Vogels¹,

Steynen²,

Maas³

et al. 1997

Journal of Hepatology

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“…Hyperammonemia is a consistent finding in human acute liver failure (ALF) as well as in experimental animal models of ALF resulting from hepatectomy (Holmin et al, 1983), hepatic devascularization (Mans et al, 1994;Swain et al, 1992a,b), or toxic liver injury (Swain et al, 1992b), and in all cases severe encephalopathy and brain edema are observed. More recently, a positive correlation was reported between arterial ammonia in acute liver failure.…”

Section: Introductionmentioning

confidence: 89%

“…Cisterna magna catheters were installed in groups of animals, as previously described (Swain et al, 1992b), 24 h after PCA or sham operation. In brief, the animal's head was mounted with the skull in a horizontal position in a stereotaxic apparatus.…”

Section: Csf Removalmentioning

confidence: 99%

“…The brain was cut into 2-mm slices, and 1-mm punch biopsy specimens were obtained from the gray matter of the cerebral cortex. Water content of each specimen was measured gravimetrically using a density gradient of bromobenzenekerosene precalibrated with K2SO4 as previously described (Swain et al, 1992b). The cortical samples were placed onto the fluid column, and the equilibration point was measured within 2 min.…”

Section: Brain Water Measurementmentioning

confidence: 99%

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Chatauret

Rose

Therrien

et al. 2001

Metabolic Brain Disease

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Chatauret, N. et al., 2001. Mild hypothermia prevents cerebral edema and CSF lactate accumulation in acute liver failure. Metabolic Brain Disease, ABSTRACT Evidence from both clinical and experimental studies demonstrates that mild hypothermia prevents encephalopathy and brain edema in acute liver failure (ALF). As part of a series of studies to elucidate the mechanism(s) involved in this protective effect, groups of rats with ALF resulting from hepatic devascularization were maintained at either 37°C (normothermic) or 35°C (hypothermic), and neurological status was monitored in relation to cerebrospinal fluid (CSF) concentrations of ammonia and lactate. CSF was removed via implanted cisterna magna catheters. Mild hypothermia resulted in a delay in onset of encephalopathy and prevention of brain edema; CSF concentrations of ammonia and lactate were concomitantly decreased. Blood ammonia concentrations, on the other hand, were not affected by hypothermia in ALF rats. These findings suggest that brain edema and encephalopathy in ALF are the consequence of ammonia-induced impairment of brain energy metabolism and open the way for magnetic resonance spectroscopic monitoring of cerebral function in ALF. Mild hypothermia could be beneficial in the prevention of severe encephalopathy and brain edema in patients with ALF awaiting liver transplantation.

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“…Glutaminase, found in neurons, produces glutamate plus ammonia from glutamine and subsequently ammonia has shown to inhibit glutaminase (Bradford et al, 1989). In addition, brain glutamate concentrations are reduced in rats with either acute (ischemic) liver failure or thioacetamide-induced liver damage (Swain et al, 1992b). Furthermore, postsynaptically, ammonia reduces the effectiveness of released glutamate (Fan et al, 1990) through AMPA receptors.…”

Section: Glutamate Release From Neuronsmentioning

confidence: 99%

Untitled

Rose

2002

Metabolic Brain Disease

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Glutamatergic dysfunction has been suggested to play an important role in the pathogenesis of hepatic encephalopathy (HE) in acute liver failure (ALF). Increased extracellular brain glutamate concentrations have consistently been described in different experimental animal models of ALF and in patients with increased intracranial pressure due to ALF. High brain ammonia levels remain the leading candidate in the pathogenesis of HE in ALF and studies have demonstrated a correlation between ammonia and increased concentrations of extracellular brain glutamate both clinically and in experimental animal models of ALF. Inhibition of glutamate uptake or increased glutamate release from neurons and/or astrocytes could cause an increase in extracellular glutamate. This review analyses the effect of ammonia on glutamate release from (and uptake into) both neurons and astrocytes and how these pathophysiological mechanisms may be involved in the pathogenesis of HE in ALF.

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Monitoring of Neurotransmitter Amino Acids by Means of An Indwelling Cisterna Magna Catheter: A Comparison of Two Rodent Models of Fulminant Liver Failure

Cited by 74 publications

References 20 publications

The effects of ammonia and portal-systemic shunting on brain metabolism, neurotransmission and intracranial hypertension in hyperammonaemia-induced encephalopathy

The effects of ammonia and portal-systemic shunting on brain metabolism, neurotransmission and intracranial hypertension in hyperammonaemia-induced encephalopathy

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