Fogel W A, Andrzejewski W, Maśliński C
Department of Biogenic Amines, Polish Academy of Sciences, Lódź.
Acta Neurobiol Exp (Wars). 1990;50(4-5):281-93.
The pathogenesis of hepatic encephalopathy (HE), a neuropsychiatric disorder resulting from liver failure, is still a matter of debate. Recently attention has been focused on brain neurotransmitters. The accumulating evidence indicates that the imbalanced metabolism and turnover as well as the altered functions of neurotransmitters (dopamine, noradrenaline, serotonin, GABA) and false neurotransmitters (phenylethanolamine, octopamine, synephrine) may be of high importance in the pathomechanism of HE. Our data permit adding histamine (HA) to the multifactorial pathogenesis of HE. The enhanced rate of histidine influx into the brain following portocaval anastomosis and a dramatic increase in the HA content in the hypothalamus may suggest the involvement of HA in the symptomatology of hepatic encephalopathy.
肝性脑病(HE)是一种由肝功能衰竭引起的神经精神障碍,其发病机制仍存在争议。最近,注意力集中在脑内神经递质上。越来越多的证据表明,神经递质(多巴胺、去甲肾上腺素、血清素、γ-氨基丁酸)和假性神经递质(苯乙醇胺、章鱼胺、辛弗林)的代谢和周转失衡以及功能改变在HE的发病机制中可能具有重要意义。我们的数据表明组胺(HA)也参与了HE的多因素发病机制。门腔静脉吻合术后组氨酸流入脑内的速率增加以及下丘脑中HA含量的显著升高,提示HA参与了肝性脑病的症状表现。