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神经传递与肝性脑病有人曾假设大脑内各种神经递质浓度发生改变是引起肝性脑病的重要机制之一。这种改变可能导致产生假性神经递质,以代替突触前神经末稍的突触前体释放的正常神经递质。这些假性神经递质包括γ-氨基丁酸、对羟苯-β-羟乙胺、5-羟色胺、组胺、苯乙胺和儿茶酚胺。已证明,在肝性脑病病人的血清及脑脊液中,上述假性神经递质都是增高的。假性神经递质对大脑有很强的抑制及刺激作用,因此对人类正常的神经递质产生具有很大的影响。
Neurotransmission and Hepatic Encephalopathy It has been hypothesized that changes in the concentration of various neurotransmitters in the brain is one of the important mechanisms responsible for hepatic encephalopathy. This change may result in the production of a pseudo-neurotransmitter in lieu of the normal neurotransmitter released by presynaptic neuropathic presynaptic precursors. These pseudo-neurotransmitters include gamma-aminobutyric acid, p-hydroxybenzene-beta-hydroxyethylamine, serotonin, histamine, phenethylamine and catecholamines. It has been demonstrated that in the serum and cerebrospinal fluid of patients with hepatic encephalopathy these false neurotransmitters are elevated. False neurotransmitters have a strong inhibitory and stimulating effect on the brain, and therefore have a great impact on normal neurotransmitter production in humans.