Update on cerebral uptake of blood ammonia
Update on cerebral uptake of blood ammonia
复制标题
血氨脑摄取的最新进展
DOI：
10.1007/s11011-013-9395-1
复制
发表时间：
2013
影响因子：
3.6
通讯作者：
M. Sørensen
中科院分区：
文献类型：
--
作者：
M. Sørensen
氨被认为在肝性脑病（HE）的发展中起着关键作用，谷氨酰胺的形成增加起着核心作用。血氨是否通过被动扩散和/或离子转运蛋白的主动转运进入大脑，以及血液pH值的变化是否会影响血氨向大脑的转移，一直存在争议。也有人提出，氨穿过血脑屏障（PSBBB）的渗透率-表面积乘积在肝硬化和HE中应增加。在本论文中，有人认为，血液pH值的变化不会改变PSBBB的氨和被动扩散与主动运输的氨的问题仍然没有得到解决。此外，最近的研究没有发现肝硬化中氨的PSBBB增加的证据。脑吸收血氨（即流量）的主要测定是动脉血氨浓度。这意味着保护大脑免受高氨血症的唯一方法是通过降低血氨，抑制大脑对氨的摄取，或通过操纵大脑氨代谢，从而减少谷氨酰胺的产生。
Ammonia is believed to play a key role in the development of hepatic encephalopathy (HE) with increased formation of glutamine playing a central role. It has been debated whether blood ammonia enters the brain by passive diffusion and/or active transport by ion-transporters and that changes in blood pH could affect the blood-to-brain transfer of ammonia. It has also been proposed that the permeability-surface area product for ammonia across the blood–brain barrier (PSBBB) should be increased in cirrhosis and HE. In the present paper it is argued that changes in blood pH does not alter PSBBB for ammonia and the question of passive diffusion versus active transport of ammonia remains unresolved. Furthermore, recent studies do not find evidence for increased PSBBB for ammonia in cirrhosis. The main determent for cerebral uptake of blood ammonia (i.e. flux) is the arterial blood ammonia concentration. This means that the only way to protect the brain from hyperammonemia is by lowering blood ammonia, inhibit cerebral uptake of ammonia, or by manipulating cerebral ammonia metabolism so that less glutamine is produced.