A carregar...
Publicação
Brain Energy Metabolism in Chronic Hepatic Encephalopathy: an in vivo and longitudinal Magnetic Resonance Spectroscopy study on a rat model of Biliary Cirrhosis
| Nome: | Descrição: | Tamanho: | Formato: | |
|---|---|---|---|---|
| 2.52 MB | Adobe PDF |
Autores
Orientador(es)
Resumo(s)
Hepatic Encephalopathy is a major neuropsychiatric syndrome that arises from acute and chronic
liver disease-induced cerebral disorders. Chronic hepatic encephalopathy is associated with cirrhosis
and stems from progressive liver brosis, thereby inducing portal hypertension and deterioration in
liver function. Hepatic encephalopathy is characterized by increased levels of ammonia, named hyperammonemia.
Given that hepatic encephalopathy induces disturbances in cerebral osmoregulation,
neurotransmission, antioxidant and energy metabolism, 1H magnetic resonance spectroscopy was performed
longitudinally on a rat model of Type C chronic hepatic encephalopathy to assess cerebral
osmolyte, energy, neurotransmitter and antioxidant metabolite concentrations. This technique was
combined with 31P Magnetic resonance spectroscopy with the purpose of measuring additional energy
metabolite concentrations. The studies were carried out at 9.4 Tesla. Rats undergone bile-duct ligation
and studies were performed at several stages of disease progression: 0, 4, 6 and 8 weeks after surgery.
Results regarding brain osmolyte concentration showed a signi cant increase in Gln, a decrease in
tChol and Ins as well as trends of decrease in Tau and Cr. These results suggest an osmoregulatory
response to the increase of Gln. In what concerns to neurotransmission, a decrease was observed in
Asp and Glu suggesting that neurotransmission is a ected by hyperammonemia which may be an
evidence of alterations in the out
ow of Gln from astrocytes and interfere with Glu synthesis. The
reduction of antioxidants Asc and GSH may indicate oxidative stress due to ammonia exposure. Small
trends of decrease observed in
-ATP and other energy metabolites which may be a sign of energy
disturbances but not signi cant to cause brain oedema. Overall, an increase in concentration levels of
Gln it is pointed as the main cause of the minimal brain oedema supported by Glutamine Hypothesis.
The results of this study are encouraging and relevant for future studies.
Descrição
Palavras-chave
Hepatic Encephalopathy chronic liver disease hyperammonemia ligation osmoregulation Glutamine Hypothesis