Henley K S, Clancy P E, Laughrey E G, Lyra L G
J Lab Clin Med. 1975 Feb;85(2):273-80.
The isolated perfused liver of the cirrhotic rat produces greater quantities of ammonia from endogenous sources or from added alanine than do control livers. It also fails to take up ammonia. In these cirrhotic livers ethanol increases ammonia production in the presence of alanine. When cirrhotic rats had received a normal diet for 10 days before perfusion, the output of ammonia from endogenous sources and from added alanine is partially restored to normal. The addition of ethanol in the presence of alanine to the perfusate of these cirrhotic livers then results in an increased rate of production of glutamine rather than of ammonia. A normal diet given these cirrhotic animals restores the uptake of ammonia to that seen in the control animals but, unlike the normal animals, the addition of ornithine increases neither the uptake of ammonia nor the output of urea. In the normal animals this effect of ornithine on the uptake of ammonia is abolished by ethanol. It is concluded that cirrhotic rat liver is a source of endogenous ammonia and that the magnitude of that contribution is modified by diet and by ethanol.
与对照肝脏相比,肝硬化大鼠的离体灌注肝脏从内源性来源或添加的丙氨酸产生的氨量更多。它也无法摄取氨。在这些肝硬化肝脏中,乙醇在有丙氨酸存在的情况下会增加氨的产生。当肝硬化大鼠在灌注前接受正常饮食10天时,内源性来源和添加丙氨酸产生的氨输出量部分恢复正常。然后,在这些肝硬化肝脏的灌注液中,在有丙氨酸存在的情况下添加乙醇会导致谷氨酰胺的产生速率增加,而不是氨的产生速率增加。给这些肝硬化动物喂食正常饮食可使氨的摄取恢复到对照动物的水平,但与正常动物不同的是,添加鸟氨酸既不会增加氨的摄取也不会增加尿素的输出。在正常动物中,乙醇会消除鸟氨酸对氨摄取的这种作用。结论是,肝硬化大鼠肝脏是内源性氨的来源,并且该贡献的大小会受到饮食和乙醇的影响。