Walle A J, Niedermayer W
Proc Eur Dial Transplant Assoc. 1980;17:162-6.
The demonstration of a sustained erythropoietin (EP) -- haematocrit (HCT) feedback mechanism would underline the importance of EP as a stimulant agent for the erythropoietic proliferation (EPRO) in chronic uraemia. Hypertransfusion showed a significant suppression of EPRO without a concomitant suppression of the pretransfusional immunodetectable (id) serum EP levels. We conclude that idEP is not the major direct mediator of EPRO in short term regulatory mechanisms in the anaemia of uraemia.
持续存在的促红细胞生成素(EP)——血细胞比容(HCT)反馈机制的证明将强调EP作为慢性尿毒症中红细胞生成增殖(EPRO)刺激剂的重要性。大量输血显示对EPRO有显著抑制作用,但对输血前免疫可检测(id)血清EP水平无相应抑制。我们得出结论,在尿毒症贫血的短期调节机制中,idEP不是EPRO的主要直接介质。