Immunohistochemical Study of the Brain Aquaporin-4 in the Rat Acute Liver Failure Model

Acute liver failure as well as acute-on-chronic liver failure result in the development of acute hepatic encephalopathy (HE) characterized by the major pathophysiologic event in form of the brain edema formation. Among brain cells, astrocytes are considered to be a central cellular population most sensitive to ammonia exposure in HE being the primarily cellular source of glutamine synthetase for ammonia metabolism. Astrocyte swelling is considered to be a principal sign of acute HE, while the exact molecular mechanisms of this event are still not fully understood. According to current concepts on HE, alteration in AQP4 regulation can play one of the central roles in the brain edema development and progression in hyperammonemia states. Considering high region-and context-specific heterogeneity of astroglial populations in the CNS, AQP4 involvement in the links of HE can also sustain mentioned conventional diversity.