Brain Aquaporin 4 in Hyperammonemia

Cauli, Omar (2010) Brain Aquaporin 4 in Hyperammonemia. Medicina universitaria, 12 (46). pp. 47-53. ISSN 1665-5796

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Resumen

In liver failure, congenital enzymopathies of the urea cycle, and other disorders, ammonia may not be properly detoxified and thus hyperammonemia ensues. Hyperammonemia is considered one of the main factors leading to cerebral edema and related consequences (increased intracranial pressure, brain herniation, and death). Cerebral edema is a critical component of neurological status impairment in patients with hyperammonemia and hepatic encephalopathy (HE). Although cerebral edema is generally classified as cytotoxic (cellular) and vasogenic (extracellular), both components often coexist in the same patient. Both types of edema can occur in acute hyperammonemia and liver failure with cytotoxic edema being a consequence of astrocytes swelling and vasogenic edema, mainly due to blood-brain barrier (BBB) disruption. It is well known that hyperammonemia is a crucial factor in astrocytes swelling and increased BBB permeability; however, the molecular mechanisms by which ammonia causes these alterations are not completely understood. Aquaporins (water channels) are one of the main pathways leading to water influx into the brain and efflux from the brain; consequently, it is conceivable brain aquaporins disturbances are involved in the pathophysiology of cerebral edema in hyperammonemia and HE. This review summarizes brain aquaporins main functions and distribution, and particularly, the aquaporin 4 (AQP-4) alterations induced under hyperammonemia and acute liver failure (ALF).

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