Mild hypothermia modifies ammonia-induced brain edema in rats after portacaval anastomosis

Background & Aims: The pathogenesis of brain edema in fulminant hepatic fai lure is still unresolved. Mild hypothermia (33 degrees-35 degrees C) can am eliorate brain edema after traumatic brain injury. We evaluated mild hypoth ermia in a model of ammonia-induced brain edema in which accumulation of br ain glutamine has been proposed as a key pathogenic factor, Methods: After portacaval anastomosis, anesthetized rats were infused with ammonium acetat e at 33 degrees, 35 degrees, and 37 degrees C or vehicle at 37 degrees C. W ater and glutamine levels in the brain, cardiac output, and regional and ce rebral hemodynamics were measured when intracranial pressure increased 3-4- fold (ammonia infusion at 37 degrees) and matched times (other groups). Res ults: Mild hypothermia reduced ammonia-induced brain swelling and increased intracranial pressure. Brain glutamine level was not decreased by hypother mia, Brain edema was accompanied by a specific increase in cerebral blood f low and oxygen consumption, which were normal in both hypothermic groups. W hen the ammonia infusion was continued in hypothermic rats, plasma ammonia levels continued to increase and brain swelling eventually developed. Concl usions: Mild hypothermia delays ammonia-induced brain edema, In this moder, an increase in cerebral perfusion is required for brain edema to become ma nifest, Mild hypothermia could be tested for treatment of intracranial hype rtension in fulminant hepatic failure.