Maddison J E
Department of Pharmacology, University of Sydney, Australia.
J Vet Intern Med. 1992 Nov-Dec;6(6):341-53. doi: 10.1111/j.1939-1676.1992.tb00367.x.
Hepatic encephalopathy occurs in a number of different species as a result of either congenital portacaval shunts or acquired liver disease. Despite intensive research, the neurochemical basis of the disorder has not been defined. Theories to explain the cerebral dysfunction that accompanies acute or chronic hepatic failure include 1) ammonia acting as the putative neurotoxin, 2) perturbed monoamine neurotransmission as a result of altered plasma amino acid metabolism, 3) an imbalance between excitatory amino acid neurotransmission, mediated by glutamate, and inhibitory amino acid neurotransmission, mediated by gamma-aminobutyric acid, and 4) increased cerebral concentrations of an endogenous benzodiazepine-like substance.
肝性脑病可因先天性门体分流或后天性肝病在多种不同物种中发生。尽管进行了深入研究，但该疾病的神经化学基础仍未明确。解释急性或慢性肝衰竭伴随的脑功能障碍的理论包括：1）氨作为假定的神经毒素；2）血浆氨基酸代谢改变导致单胺神经传递紊乱；3）由谷氨酸介导的兴奋性氨基酸神经传递与由γ-氨基丁酸介导的抑制性氨基酸神经传递之间失衡；4）内源性苯二氮䓬类物质的脑内浓度增加。
