Waterlow J C, Jackson A A, Golden M H, Jahoor F, Sutton G, Fern E B
Department of Public Health and Policy, London School of Hygiene and Tropical Medicine.
Br J Nutr. 1994 Jul;72(1):83-92. doi: 10.1079/bjn19940011.
In three experiments [amide-15N]glutamine was infused intravenously in male volunteers. After 4-8 h of infusion acidosis was achieved by an oral dose of CaCl2 (1 mmol/kg). In one subject acidosis was maintained for 5 d. The acid load produced an approximately 3-fold increase in urinary NH3 excretion, with a small (approximately 20%) and transient increase in the isotope abundance of urinary NH3. Estimates of glutamine production rate (flux) were obtained in two experiments. There was no evidence that it was increased in acidosis. The extra NH3 production by the kidney represented only a very small part, about 3%, of the total glutamine production rate.
在三项实验中,向男性志愿者静脉输注[酰胺 - 15N]谷氨酰胺。输注4 - 8小时后,通过口服氯化钙(1 mmol/kg)诱发酸中毒。在一名受试者中,酸中毒持续了5天。酸负荷使尿氨排泄量增加了约3倍,同时尿氨的同位素丰度有小幅(约20%)且短暂的增加。在两项实验中获得了谷氨酰胺生成率(通量)的估计值。没有证据表明在酸中毒时其会增加。肾脏额外产生的氨仅占谷氨酰胺总生成率的很小一部分,约为3%。