Friolet R, Colombo J P, Lazeyras F, Aue W P, Kretschmer R, Zimmermann A, Bachmann C
Department of Clinical Chemistry, Inselspital, Switzerland.
Biochem Biophys Res Commun. 1989 Mar 15;159(2):815-20. doi: 10.1016/0006-291x(89)90067-3.
Hyperammonemia is a major contributing factor to the neurological abnormalities observed in hepatic encephalopathy and in congenital defects of ammonia detoxication. In rats variable changes in labile energy rich phosphates in the brain have been observed in hyperammonemia using biochemical methods. Using 31P-NMR spectroscopy however no significant changes of the relative concentrations of the energy rich phosphates alpha, beta and gamma-ATP, phosphocreatine, inorganic phosphate and the pH were found in the fronto parietal cortex of the urease treated hyperammonemic rat. Alterations in the metabolites of these compounds do not appear to be a major pathomechanism of ammonia toxicity in this brain area.
高氨血症是在肝性脑病和先天性氨解毒缺陷中观察到的神经功能异常的主要促成因素。在大鼠中,使用生化方法已观察到高氨血症时大脑中不稳定的富含能量的磷酸盐有多种变化。然而,使用31P-NMR光谱法,在经脲酶处理的高氨血症大鼠的额顶叶皮质中,未发现富含能量的磷酸盐α、β和γ-ATP、磷酸肌酸、无机磷酸盐的相对浓度以及pH有显著变化。这些化合物代谢产物的改变似乎不是该脑区氨毒性的主要发病机制。