BRAIN AQP4 DURING EXPERIMENTAL ACUTE LIVER FAILURE

Hepatic encephalopathy (HE) was defined as a complex neuropsychiatric syndrome triggered by severe liver pathology and manifesting covert overt alterations up to hepatic coma death [1]. Acute failure (ALF) results in acute (AHE) characterized brain edema caused mechanisms closely linked ammonia toxicity [2]. Astrocytes are central cells the most sensitive being primarily source of glutamine synthetase (GS), therefore astrocyte swelling is principal feature AHE [1-3]. Aquaporin-4 (AQP4) one molecules responsible for water homeostasis cell volume health disease presents abundant channel CNS. According current HE pathophysiology, alteration AQP4 regulation can play role progression Considering high heterogeneity astroglia populations CNS, involvement links also sustain mentioned conventional diversity. The purpose study determining level different rat regions conditions ALF.