Torremans A, D'Hooge R, Van de Vijver G, Marescau B, Vanholder R, Lameire N, De Deyn P P, Van Bogaert P P
Laboratory of Neurochemistry and Behaviour/Born Bunge Foundation, University of Antwerp, Universiteitsplein 1, B-2610 Antwerp (Wilrijk), Belgium.
Brain Res. 2004 May 15;1008(1):107-12. doi: 10.1016/j.brainres.2004.02.021.
Uremic retention solutes possibly contribute to neuronal hypoxia/ischemia and its consequences in patients with renal failure. We examined the in vitro effects of several uremic retention solutes on murine central neurons under chemically induced metabolic hypoxia by application of sodium cyanide (NaCN). Whole cell currents were recorded using the tight-seal whole-cell voltage clamp technique. Application of NaCN caused an inward whole-cell current. From all tested toxins, which included several indoles, guanidino compounds, polyamines, purines, phenols, DL-homocysteine, orotate and myoinositol, only creatinine (CTN), guanidine (G) and guanidinosuccinic acid (GSA) produced a significant current in control and hypoxic neurons. Current evoked by GSA was significantly increased in the chemical hypoxic condition, and a synergistic effect of GSA and spermine was observed in hypoxic neurons.
尿毒症潴留溶质可能导致肾衰竭患者的神经元缺氧/缺血及其后果。我们通过应用氰化钠（NaCN）在化学诱导的代谢性缺氧条件下，研究了几种尿毒症潴留溶质对小鼠中枢神经元的体外影响。使用紧密封接全细胞电压钳技术记录全细胞电流。应用NaCN引起内向全细胞电流。在所有测试的毒素中，包括几种吲哚、胍基化合物、多胺、嘌呤、酚类、DL-同型半胱氨酸、乳清酸盐和肌醇，只有肌酐（CTN）、胍（G）和胍基琥珀酸（GSA）在对照和缺氧神经元中产生显著电流。在化学缺氧条件下，GSA诱发的电流显著增加，并且在缺氧神经元中观察到GSA和精胺的协同作用。
