Le rôle du stress oxydatif/nitrosatif dans la pathogénèse de l’encéphalopathie hépatique chronique
Hepatic encephalopathy (HE) is a neuropsychiatric complication due to liver failure where ammonia is believed to be central in the pathogenesis. Acute ammonia intoxication has demonstrated to induce oxidative/nitrosative stress in both in vivo and in vitro models. The present study was aimed to assess the role of oxidative/nitrosative stress in 2 models of chronic liver failure/HE; 1. portacaval anastomosis (PCA) and 2. bile duct ligation (BDL). Both models are characterised with hyperammonemia and increased brain ammonia however cerebral edema is only found in BDL rats. Oxidative/nitrosative stress markers were evaluated in plasma and frontal cortex of both animal models. Central nitrosative stress was observed in PCA rats, but systemic oxidative/ntrosative stress was demonstrated only in BDL rats. The results of our study suggest i) chronic hyperammonemia does not induce oxidative stress and ii) a synergistic effect between ammonia and systemic oxidative/nitrosative stress is associated with cerebral edema.
Minimal hepatic encephalopathy (MHE) Hyperammonemia Anastomose portocave (portacaval anastomosis PCA) Portacaval anastomosis (PCA) Bile duct ligation (BDL) Oxidative/nitrosative stress Cerebral edema