Brain lactate by magnetic resonance spectroscopy during fulminant hepatic failure in the dog.

Détails

ID Serval
serval:BIB_86C36586EF9C
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Brain lactate by magnetic resonance spectroscopy during fulminant hepatic failure in the dog.
Périodique
Liver Transplantation and Surgery
Auteur(s)
Nyberg S.L., Cerra F.B., Gruetter R.
ISSN
1527-6465; 1074-3022 (Print)
ISSN-L
1074-3022
Statut éditorial
Publié
Date de publication
1998
Volume
4
Numéro
2
Pages
158-165
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.Publication Status: ppublish
Résumé
A noninvasive test is needed to assess the severity of encephalopathy during fulminant hepatic failure. This feasibility study was designed to compare a noninvasive test, brain lactate measurement by magnetic resonance spectroscopy, with intracranial pressure monitoring in a large animal model of fulminant hepatic failure. Five dogs received an intraventricular catheter for intracranial pressure measurement. Liver injury was induced by intravenous bolus of D-galactosamine. Brain lactate concentrations were determined by magnetic resonance spectroscopy for up to 48 hours after D-galactosamine administration (t = 0 hour). A dose of D-galactosamine exceeding 1.5 g/kg resulted in fulminant hepatic failure. Brain lactate levels increased to > 10 mmol/L in the two dogs that developed severe intracranial hypertension of > 50 mm Hg and sustained cerebral perfusion pressures of < 40 mm Hg. Both dogs experienced brain death, 42 and 48 hours after the administration of D-galactosamine. Brain lactate concentrations determined by magnetic resonance spectroscopy were in agreement with brain tissue concentrations of lactate determined by high-performance liquid chromatography at necropsy. Plasma lactate concentrations were only mildly elevated (3.2 and 4.2 mmol/L) at the time of brain death. Elevated levels of brain lactate are associated with intracranial hypertension and poor neurological outcome during fulminant hepatic failure.
Mots-clé
Animals, Biological Markers/analysis, Brain/metabolism, Dogs, Dose-Response Relationship, Drug, Feasibility Studies, Galactosamine/pharmacology, Glutamic Acid/metabolism, Glutamine/metabolism, Hepatic Encephalopathy/chemically induced, Hepatic Encephalopathy/metabolism, Intracranial Hypertension/physiopathology, Lactic Acid/blood, Lactic Acid/metabolism, Magnetic Resonance Spectroscopy, Male, Time Factors
Pubmed
Création de la notice
04/08/2010 16:28
Dernière modification de la notice
03/03/2018 19:00
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