Denays R, Chao S L, Mathur-Devré R, Jeghers O, Frühling J, Noël P, Ham H R
Department of Neurology, St-Pierre Hospital, Brussels, Belgium.
Magn Reson Med. 1993 Jun;29(6):719-23. doi: 10.1002/mrm.1910290602.
In this work, 31P phosphorus NMR (31P NMR) studies of the brain have been conducted in rats acutely and chronically intoxicated with ethanol. In both groups, changes in levels of high-energy phosphates were observed: increase of phosphocreatinine (PCr)/beta AaTP and PCr/inorganic phosphate (Pi) in acute and long-term ethanol exposure, and decrease of Pi/beta ATP after acute ethanol administration. These changes in high-energy phosphates, indicative of a reduction of adenosine triphosphate (ATP) and PCr consumption (PCr+ ADP+ H+ ATP+ Cr; ATP ADP+ Pi), suggest a reduction of cerebral metabolism both in acute and chronic ethanol exposure. In addition, in the group of rats chronically intoxicated with ethanol, there were variations in phosphodiester peak intensities (decrease of phosphomonoester (PME)/phosphodiester (PDE), increase of PDE/beta ATP), suggesting increased breakdown of membrane phospholipids. These changes could provide a metabolic explanation for the development of cerebral atrophy in chronic alcoholism.
在这项研究中，对急性和慢性乙醇中毒的大鼠进行了大脑的31P磷核磁共振（31P NMR）研究。在两组中，均观察到高能磷酸盐水平的变化：急性和长期乙醇暴露后磷酸肌酸（PCr）/β-ATP和PCr/无机磷酸盐（Pi）升高，急性乙醇给药后Pi/β-ATP降低。这些高能磷酸盐的变化表明三磷酸腺苷（ATP）和PCr消耗减少（PCr+ADP+H+⇌ATP+Cr；ATP⇌ADP+Pi），提示急性和慢性乙醇暴露时脑代谢均降低。此外，在慢性乙醇中毒的大鼠组中，磷酸二酯峰强度存在变化（磷酸单酯（PME）/磷酸二酯（PDE）降低，PDE/β-ATP升高），提示膜磷脂分解增加。这些变化可为慢性酒精中毒时脑萎缩的发生提供代谢方面的解释。
