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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Interorgan ammonia metabolism in liver failure.
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Interorgan ammonia metabolism in liver failure.

机译：肝衰竭中的器官间氨代谢。

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In the post-absorptive state, ammonia is produced in equal amounts in the small and large bowel. Small intestinal synthesis of ammonia is related to amino acid breakdown, whereas large bowel ammonia production is caused by bacterial breakdown of amino acids and urea. The contribution of the gut to the hyperammonemic state observed during liver failure is mainly due to portacaval shunting and not the result of changes in the metabolism of ammonia in the gut. Patients with liver disease have reduced urea synthesis capacity and reduced peri-venous glutamine synthesis capacity, resulting in reduced capacity to detoxify ammonia in the liver.The kidneys produce ammonia but adapt to liver failure in experimental portacaval shunting by reducing ammonia release into the systemic circulation. The kidneys have the ability to switch from net ammonia production to net ammonia excretion, which is beneficial for the hyperammonemic patient. Data in experimental animals suggest that the kidneys could have a major role in post-feeding and post-haemorrhagic hyperammonemia.During hyperammonemia, muscle takes up ammonia and plays a major role in (temporarily) detoxifying ammonia to glutamine. Net uptake of ammonia by the brain occurs in patients and experimental animals with acute and chronic liver failure. Concomitant release of glutamine has been demonstrated in experimental animals, together with large increases of the cerebral cortex ammonia and glutamine concentrations. In this review we will discuss interorgan trafficking of ammonia during acute and chronic liver failure. Interorgan glutamine metabolism is also briefly discussed, since glutamine synthesis from glutamate and ammonia is an important alternative pathway of ammonia detoxification. The main ammonia producing organs are the intestines and the kidneys, whereas the major ammonia consuming organs are the liver and the muscle.
机译：在吸收后的状态下，大小肠中的氨含量相同。小肠中氨的合成与氨基酸分解有关，而大肠氨的产生是由氨基酸和尿素的细菌分解引起的。在肝衰竭期间观察到的肠对高氨血症状态的贡献主要是由于门腔分流引起的，而不是肠中氨代谢变化的结果。患有肝病的患者尿素合成能力降低，静脉谷氨酰胺合成能力降低，从而使肝脏中的氨解毒能力降低。肾脏产生氨，但通过减少门静脉分流到系统循环中的氨来适应实验性门腔分流术中的肝衰竭。肾脏有能力从净氨生成转换为净氨排泄，这对高氨血症患者有益。实验动物的数据表明，肾脏可能在喂养后和出血性高氨血症中起主要作用。在高氨血症期间，肌肉吸收氨并在（暂时）将氨解毒为谷氨酰胺中起主要作用。在急性和慢性肝功能衰竭的患者和实验动物中，大脑会净吸收氨。已经在实验动物中证明了谷氨酰胺的伴随释放，以及大脑皮层中氨和谷氨酰胺浓度的大幅增加。在这篇综述中，我们将讨论急性和慢性肝衰竭期间氨的器官间运输。由于由谷氨酸和氨合成谷氨酰胺是氨解毒的重要替代途径，因此还简要讨论了器官间谷氨酰胺代谢。产生氨的主要器官是肠和肾，而消耗氨的主要器官是肝脏和肌肉。

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