Capocaccia L, Cangiano C, Attili A F, Angelico M, Cascino A, Rossi Fanelli F
Clin Chim Acta. 1977 Feb 15;75(1):99-105. doi: 10.1016/0009-8981(77)90504-6.
It has been recently proposed that hepatic encephalopathy could be due to the accumulation of octopamine acting as a false neurotransmitter, and the increase of ammonia might reflect this accumulation. The simultaneous determination of octopamine and ammonia was performed in 88 cases with or without encephalopathy. The correlation between the two substances appeared to be good (P less than 0.01; r = 0.5), except in shunted patients. All the cases with low octopamine and high ammonia were patients who had been submitted to surgical portal-systemic anastomosis. This finding does not seem to be coincidental; in this type of patients, the mechanism of hepatic encephalopathy could involve other beta-hydroxyphenylethanolamines in addition to octopamine. The presence of the inhibition of the reaction of transmethylation constantly observed during octopamine plasma assay is in favour of this hypothesis.
最近有人提出,肝性脑病可能是由于作为假神经递质的章鱼胺积累所致,而氨的增加可能反映了这种积累。对88例有或无脑病的患者同时测定了章鱼胺和氨。除分流患者外,这两种物质之间的相关性似乎良好(P<0.01;r=0.5)。所有章鱼胺水平低而氨水平高的病例都是接受过外科门体分流吻合术的患者。这一发现似乎并非巧合;在这类患者中,肝性脑病的机制可能除了章鱼胺外还涉及其他β-羟基苯乙醇胺。在章鱼胺血浆检测过程中经常观察到的转甲基反应抑制的存在支持了这一假设。