Monti J P, Baz M, Elsen R, Berland Y F, Crevat A D
Laboratoire de Biophysique, Faculté de Pharmacie, Université d'Aix-Marseille II.
Biochim Biophys Acta. 1990 Aug 10;1027(1):31-40. doi: 10.1016/0005-2736(90)90044-o.
Cation transport in erythrocytes of some uremic patients is impaired. Most studies have focused on the defect of the erythrocyte Na+/K+ pump in these diseased states. Herein, this cation transport defect was studied by using nuclear magnetic resonance spectroscopy (NMR) which is a non-invasive method permitting study on living erythrocytes. Firstly, we verified that the Na+ transport defect in uremic erythrocytes was not due to non-specific causes such as membrane alteration or a modification of the intracellular metabolism. The proton relaxation data, determined using a paramagnetic doping method, are consistent with a lack of erythrocytic membrane damage in uremic patients. Also, 31P-NMR results showed that in our experimental conditions, uremic and normal erythrocytes exhibit similar variations of ATP level over time. Lastly, the use of anionic paramagnetic shift reagent in 23Na-NMR revealed a defect in the Na+/K+ pump of erythrocytes from uremic patients with high Nain concentration. This defect seems to be due to a reduced number of pump units and to the presence of an endogenous inhibitor in uremic plasma.
一些尿毒症患者红细胞中的阳离子转运受损。大多数研究都集中在这些患病状态下红细胞钠钾泵的缺陷上。在此，通过使用核磁共振波谱法（NMR）来研究这种阳离子转运缺陷，这是一种非侵入性方法，可用于研究活红细胞。首先，我们证实尿毒症红细胞中的钠转运缺陷并非由非特异性原因引起，如膜改变或细胞内代谢的改变。使用顺磁掺杂法测定的质子弛豫数据与尿毒症患者红细胞膜无损伤一致。此外，31P-NMR结果表明，在我们的实验条件下，尿毒症红细胞和正常红细胞随时间推移ATP水平呈现相似变化。最后，在23Na-NMR中使用阴离子顺磁位移试剂揭示了高钠浓度的尿毒症患者红细胞钠钾泵存在缺陷。这种缺陷似乎是由于泵单元数量减少以及尿毒症血浆中存在内源性抑制剂所致。
