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高氨血症期间大鼠门静脉引流内脏和后肢的谷氨酰胺代谢改变。

Altered glutamine metabolism in rat portal drained viscera and hindquarter during hyperammonemia.

作者信息

Dejong C H, Kampman M T, Deutz N E, Soeters P B

机构信息

Department of Surgery, University of Limburg, Maastricht, The Netherlands.

出版信息

Gastroenterology. 1992 Mar;102(3):936-48. doi: 10.1016/0016-5085(92)90180-7.

Abstract

In normal rats, muscle is the major glutamine releasing organ and gut is the major glutamine consuming organ. It has been suggested that enhanced muscle ammonia detoxification and gut ammonia production occurs during liver insufficiency-induced hyperammonemia. Therefore, ammonia and amino acid fluxes across portal-drained viscera and hindquarter, and muscle concentrations were measured in portacaval shunted and acute liver ischemia rats. Arterial ammonia and most amino acids were increased after portacaval shunting and increased progressively during liver ischemia, but net hindquarter ammonia uptake was not observed. Net hindquarter glutamine efflux was increased during portacaval shunting, but it decreased during liver ischemia, while muscle glutamine concentrations increased. The comparable net portal drained viscera glutamine uptake in normal and portacaval shunted rats changed during liver ischemia from net uptake to release, coinciding with release of most other amino acids. These results cast doubt on the ammonia detoxifying role of muscle during acute liver ischemia-induced hyperammonemia in the rat. The portal drained viscera glutamine release during severe hyperammonemia could be due to intestinal damage.

摘要

在正常大鼠中,肌肉是主要的谷氨酰胺释放器官,而肠道是主要的谷氨酰胺消耗器官。有人提出,在肝功能不全诱导的高氨血症期间,肌肉氨解毒作用增强,肠道氨生成增加。因此,在门腔分流和急性肝缺血大鼠中,测量了流经门脉引流内脏和后肢的氨和氨基酸通量以及肌肉浓度。门腔分流后动脉血氨和大多数氨基酸增加,在肝缺血期间逐渐升高,但未观察到后肢净氨摄取。门腔分流期间后肢谷氨酰胺净流出增加,但在肝缺血期间减少,而肌肉谷氨酰胺浓度增加。正常大鼠和门腔分流大鼠门脉引流内脏谷氨酰胺净摄取相当,在肝缺血期间从净摄取变为释放,与大多数其他氨基酸的释放一致。这些结果对大鼠急性肝缺血诱导的高氨血症期间肌肉的氨解毒作用提出了质疑。严重高氨血症期间门脉引流内脏谷氨酰胺的释放可能是由于肠道损伤。

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