title: Mild hypothermia in the prevention of brain edema in acute liver failure: mechanisms and clinical prospects.
abstract: Mild hypothermia (32 degrees C-35 degrees C) reduces intracranial pressure in patients with acute liver failure and may offer an effective adjunct therapy in the management of these patients. Studies in experimental animals suggest that this beneficial effect of hypothermia is the result of a decrease in blood-brain ammonia transfer resulting in improvement in brain energy metabolism and normalization of glutamatergic synaptic regulation. Improvement in brain energy metabolism by hypothermia may result from a reduction in ammonia-induced decrease of brain glucose (pyruvate) oxidation. Restoration of normal glutamatergic synaptic regulation by hypothermia may be the consequence of the removal of ammonia-induced decreases in expression of astrocytic glutamate transporters resulting in normal glutamate neurotransmitter inactivation in brain. Randomized controlled clinical trials of hypothermia are required to further evaluate its clinical impact.
authors.affiliation: Neuroscience Research Unit, C.H.U.M. (Hôpital Saint-Luc), University of Montreal, Montreal, Quebec, Canada.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Chatauret
authors.forename: Christopher
authors.initials: C
authors.lastname: Rose
authors.forename: Roger F
authors.initials: RF
authors.lastname: Butterworth
mesh_terms: D000641:Ammonia / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D001929:Brain Edema / Q000517:prevention & control*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D007036:Hypothermia, Induced; D019344:Lactic Acid / Q000378:metabolism; D017114:Liver Failure, Acute / Q000378:metabolism / Q000628:therapy*
chemical_list: D019344:Lactic Acid; D018698:Glutamic Acid; D000641:Ammonia