Thomas T H, Mansy H, Wilkinson R
Department of Medicine, University of Newcastle upon Tyne, UK.
Nephrol Dial Transplant. 1989;4(1):21-6.
Erythrocyte sodium and sodium fluxes in plasma and in physiological buffer solution were studied in normotensive and hypertensive uraemic patients and normal subjects. Erythrocyte sodium was reduced in the uraemic patients due primarily to low sodium influx, further supported by low passive membrane permeability. These differences were much more marked in normotensive patients. There was no evidence for sodium pump inhibition in the erythrocytes. The low erythrocyte sodium influx in the uraemic patients appeared to be due to a plasma factor which could be reversed in young cells but not in old. However, erythrocyte sodium flux in both plasma and physiological buffer was lower in normotensive than in hypertensive uraemic patients. Therefore, a membrane change to compensate for the effects of the plasma factor on sodium influx may be related to the development of hypertension in the uraemic patients.
对血压正常和高血压的尿毒症患者以及正常受试者的红细胞钠、血浆及生理缓冲溶液中的钠通量进行了研究。尿毒症患者红细胞钠减少主要是由于钠内流低，低被动膜通透性进一步支持了这一点。这些差异在血压正常的患者中更为明显。没有证据表明红细胞中钠泵受到抑制。尿毒症患者红细胞钠内流低似乎是由于一种血浆因子，这种因子在年轻细胞中可逆转，但在衰老细胞中不可逆转。然而，血压正常的尿毒症患者血浆和生理缓冲液中的红细胞钠通量均低于高血压尿毒症患者。因此，为补偿血浆因子对钠内流的影响而发生的膜变化可能与尿毒症患者高血压的发生有关。
