The brain in acute liver failure. A tortuous path from hyperammonemia to cerebral edema

被引：59

作者：

Bjerring, Peter Nissen ^{[1
]}

Eefsen, Martin ^{[1
]}

Hansen, Bent Adel ^{[1
]}

Larsen, Fin Stolze ^{[1
]}

机构：

[1] Univ Copenhagen Hosp, Rigshosp, Dept Hepatol, Sect A 2121, DK-2100 Copenhagen, Denmark

来源：

METABOLIC BRAIN DISEASE | 2009年 / 24卷 / 01期

关键词：

Acute liver failure; Cerebral edema; Hyperammonemia; Intracranial hypertension; FULMINANT HEPATIC-FAILURE; MITOCHONDRIAL PERMEABILITY TRANSITION; BLOOD-FLOW AUTOREGULATION; CULTURED ASTROCYTES; INTRACRANIAL HYPERTENSION; PORTACAVAL ANASTOMOSIS; GLUTAMINE-SYNTHETASE; AMMONIA METABOLISM; OXIDATIVE STRESS; AMINO-ACIDS;

D O I：

10.1007/s11011-008-9116-3

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Acute liver failure (ALF) is a condition with an unfavourable prognosis. Multiorgan failure and circulatory collapse are frequent causes of death, but cerebral edema and intracranial hypertension (ICH) are also common complications with a high risk of fatal outcome. The underlying pathogenesis has been extensively studied and although the development of cerebral edema and ICH is of a complex and multifactorial nature, it is well established that ammonia plays a pivotal role. This review will focus on the effects of hyperammonemia on neurotransmission, mitochondrial function, oxidative stress, inflammation and regulation of cerebral blood flow. Finally, potential therapeutic targets and future perspectives are briefly discussed.

引用

页码：5 / 14

页数：10

共 68 条

[31] Sources of oxygen radicals in brain in acute ammonia intoxication in vivo [J].