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Bile-duct ligation renders the brain susceptible to hypotension-induced neuronal degeneration: Implications of ammonia.
Clément, Marc-André; Bosoi, Cristina R; Oliveira, Mariana M; Tremblay, Mélanie; Bémeur, Chantal; Rose, Christopher F.
Afiliación
  • Clément MA; Hepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montréal, Canada.
  • Bosoi CR; Hepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montréal, Canada.
  • Oliveira MM; Hepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montréal, Canada.
  • Tremblay M; Hepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montréal, Canada.
  • Bémeur C; Hepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montréal, Canada.
  • Rose CF; Hepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montréal, Canada.
J Neurochem ; 157(3): 561-573, 2021 05.
Article en En | MEDLINE | ID: mdl-33382098
Hepatic encephalopathy (HE) is a debilitating neurological complication of cirrhosis. By definition, HE is considered a reversible disorder, and therefore HE should resolve following liver transplantation (LT). However, persisting neurological complications are observed in as many as 47% of LT recipients. LT is an invasive surgical procedure accompanied by various perioperative factors such as blood loss and hypotension which could influence outcomes post-LT. We hypothesize that minimal HE (MHE) renders the brain frail and susceptible to hypotension-induced neuronal cell death. Six-week bile duct-ligated (BDL) rats with MHE and respective SHAM-controls were used. Several degrees of hypotension (mean arterial pressure of 30, 60 and 90 mm Hg) were induced via blood withdrawal from the femoral artery and maintained for 120 min. Brains were collected for neuronal cell count and apoptotic analysis. In a separate group, BDL rats were treated for MHE with the ammonia-lowering strategy ornithine phenylacetate (OP; MNK-6105), administered orally (1 g/kg) for 3 weeks before induction of hypotension. Hypotension 30 and 60 mm Hg (not 90 mm Hg) significantly decreased neuronal marker expression (NeuN) and cresyl violet staining in the frontal cortex compared to respective hypotensive SHAM-operated controls as well as non-hypotensive BDL rats. Neuronal degeneration was associated with an increase in cleaved caspase-3, suggesting the mechanism of cell death was apoptotic. OP treatment attenuated hyperammonaemia, improved anxiety and activity, and protected the brain against hypotension-induced neuronal cell death. Our findings demonstrate that rats with chronic liver disease and MHE are more susceptible to hypotension-induced neuronal cell degeneration. This highlights MHE at the time of LT is a risk factor for poor neurological outcome post-transplant and that treating for MHE pre-LT might reduce this risk.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Conductos Biliares / Enfermedades Neurodegenerativas / Amoníaco / Hipotensión / Neuronas Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: J Neurochem Año: 2021 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Conductos Biliares / Enfermedades Neurodegenerativas / Amoníaco / Hipotensión / Neuronas Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Animals Idioma: En Revista: J Neurochem Año: 2021 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido