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Brain magnetic resonance in experimental acute‐on‐chronic liver failure
Author(s) -
Chavarria Laia,
Oria Marc,
RomeroGiménez Jordi,
Alonso Juli,
LopePiedrafita Silvia,
Cordoba Juan
Publication year - 2013
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/liv.12032
Subject(s) - medicine , pathology , magnetic resonance imaging , in vivo magnetic resonance spectroscopy , liver disease , decompensation , hepatic encephalopathy , endocrinology , cirrhosis , radiology
Background & Aim Acute‐on‐chronic liver failure is the term that refers to sustained liver injury with acute decompensation, usually induced by a precipitating factor. A common link between ensuing failures of various organs is impairment of the vascular supply, which may also induce vasogenic oedema in the brain. The aim of this study was to perform magnetic resonance ( MR ) study of the brain in a rat model combining bile duct ligation ( BDL ) and lipopolysaccharide ( LPS ) administration to investigate brain oedema in liver failure. Methods Bile duct‐ligated rats underwent in vivo brain MR imaging at 4, 5 and 6 weeks, and after superimposed administration of LPS . The MR techniques applied enabled assessment of brain metabolites, and intra‐ or extracellular water distribution. Brain water content was assessed by gravimetry. Results MR spectroscopy showed an increase in brain glutamine and a decrease in myo‐inositol and choline in relation to progression of liver disease. BDL rats showed a slight, progressive increase in the amount of cortical brain water that was significant after LPS injection. These changes did not modify the apparent diffusion coefficient, supporting a mixed origin of brain oedema (vasogenic and cytotoxic). Conclusions The mechanisms leading to the development of brain oedema in an experimental liver disease model were related to the time course of liver failure and to pro‐inflammatory stimuli. MR findings support the presence of cytotoxic and vasogenic mechanisms in induced brain oedema in BDL rats exposed to LPS .