Suppr超能文献

急性氨中毒对脑网状激活系统能量储备的影响。

Effect of acute ammonia intoxication on energy stores in the cerebral reticular activating system.

作者信息

McCandless D W, Schenker S

出版信息

Exp Brain Res. 1981;44(3):325-30. doi: 10.1007/BF00236570.

Abstract

Ammonia intoxication causes loss of consciousness. One postulated mechanism for this stipulates impaired energy metabolism in critical brain sites. The ascending reticular activating system in the brainstem may modulate consciousness. Accordingly, the present study, using micromethods, assessed energy stores in cells from the reticular activating system of mice acutely intoxicated with ammonia. In the early coma period (3.5 min after ammonia) phosphocreatine, adenosine triphosphate and glucose fell significantly while glycogen decreased later. Subsequently during coma, the high energy phosphates returned to normal and supranormal. The maximal fall in these metabolites was not accompanied by a rise in lactate, implying lack of local hypoxia or acidosis. The cells of the posterior coliculus in the same animals failed to show a significant fall in energy stores. These data suggest a selective effect of ammonia on energy metabolism in the cells of the reticular activating system of the brainstem.

摘要

氨中毒会导致意识丧失。一种对此现象的假设机制认为,关键脑区的能量代谢受损。脑干中的上行网状激活系统可能调节意识。因此,本研究采用微量法,评估了急性氨中毒小鼠网状激活系统细胞中的能量储备。在昏迷早期(氨中毒后3.5分钟),磷酸肌酸、三磷酸腺苷和葡萄糖显著下降,而糖原稍后减少。随后在昏迷期间,高能磷酸盐恢复到正常和超常水平。这些代谢物的最大降幅并未伴随着乳酸的升高,这意味着不存在局部缺氧或酸中毒。同一动物后丘的细胞未显示出能量储备的显著下降。这些数据表明氨对脑干网状激活系统细胞的能量代谢具有选择性作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验