Michael J, Hilton P J, Jones N F
Am J Clin Nutr. 1978 Oct;31(10):1945-7. doi: 10.1093/ajcn/31.10.1945.
A defect in sodium transport is known to exist in the leucocytes of uremic patients. Recent work has shown changes in cation flux rates associated with alterations of extracellular zinc concentration. As plasma zinc is known to be low in uremia, the possibility that this might be the cause of the defect in membrane transport was investigated. Plasma zinc was shown to be lower in uremic patients than in normal controls but this was not matched by alterations in leucocyte zinc content. Leucocytes from normal subjects and from patients with uremia have similar increases in the sodium efflux rate constant when exposed to elevated extracellular zinc concentrations. However, the abnormality in leucocyte sodium transport in uremia was not completely corrected by elevation of the extracellular zinc, when compared with normal cells in the same zinc concentrations. Although extracellular zinc is a factor that must be controlled in studies of cellular membrane transport, a low plasma zinc is not the explanation for the defect of sodium transport seen in uremia.
已知尿毒症患者的白细胞存在钠转运缺陷。最近的研究表明，阳离子通量率的变化与细胞外锌浓度的改变有关。由于已知尿毒症患者血浆锌含量较低，因此研究了这可能是膜转运缺陷原因的可能性。结果显示，尿毒症患者的血浆锌含量低于正常对照组，但白细胞锌含量并未相应改变。正常受试者和尿毒症患者的白细胞在暴露于升高的细胞外锌浓度时，钠流出速率常数有类似增加。然而，与相同锌浓度下的正常细胞相比，尿毒症患者白细胞钠转运异常并未因细胞外锌升高而完全纠正。尽管在细胞膜转运研究中必须控制细胞外锌这一因素，但血浆锌含量低并不能解释尿毒症患者所见的钠转运缺陷。
