Welbourne T C
Metabolism. 1986 Jul;35(7):614-8. doi: 10.1016/0026-0495(86)90166-6.
The relationship between hindquarter glutamine release and renal glutamine extraction was studied in rats undergoing chronic metabolic acidosis. Metabolic acidosis was induced by maintaining rats on NH4CL for four days; controls were pair-fed NH4HCO3. Metabolic acidosis increased renal glutamine extraction 8-fold and decreased arterial plasma glutamine concentration 40%. Hindquarter glutamine release rose 5-fold in acidosis due to an increased arteriovenous glutamine concentration difference and a significant rise in blood flow through the hindquarters. Both ammonia and glutamate extraction in the hindquarter increased in acidosis and could account for 25% of the glutamine nitrogen released. Alanine release by hindquarters, which exceeded glutamine release in the control animals, was greatly depressed in metabolic acidosis. The reduction in alanine nitrogen release during acidosis could account for 25% of the glutamine nitrogen released. Consequently, metabolic acidosis stimulates hindquarter glutamine release at the expense of alanine and is also supported by greater extraction of ammonia and glutamate. However, other N sources must supply nearly 50% of the glutamine nitrogen released based on balance studies.
在患有慢性代谢性酸中毒的大鼠中，研究了后肢谷氨酰胺释放与肾脏谷氨酰胺摄取之间的关系。通过让大鼠连续四天摄入氯化铵来诱导代谢性酸中毒；对照组则配对喂食碳酸氢铵。代谢性酸中毒使肾脏谷氨酰胺摄取增加了8倍，并使动脉血浆谷氨酰胺浓度降低了40%。由于动静脉谷氨酰胺浓度差增加以及后肢血流量显著增加，酸中毒时后肢谷氨酰胺释放增加了5倍。酸中毒时后肢的氨和谷氨酸摄取均增加，且可占释放的谷氨酰胺氮的25%。后肢丙氨酸释放量在对照组动物中超过谷氨酰胺释放量，但在代谢性酸中毒时大幅降低。酸中毒期间丙氨酸氮释放量的减少可占释放的谷氨酰胺氮的25%。因此，代谢性酸中毒以丙氨酸为代价刺激后肢谷氨酰胺释放，并且也受到氨和谷氨酸摄取增加的支持。然而，根据平衡研究，其他氮源必须提供近50%的释放的谷氨酰胺氮。
