Recent investigations employing various ionophores and cardiac glycosides have detected an increase in the number of late-stage erythroid progenitor cells (CFU-e) cultured from normal murine marrow. We report that the cardiac glycoside, ouabain, not only increased the number of erythroid progenitor cells, but also elevated the number of the earliest erythroid colony-forming cells (BFU-e). This rise in the number of erythroid stem cells was dose dependent with a maximum increase in erythroid colony numbers observed at 10(-15) M ouabain. Furthermore, ouabain exerted its stimulatory activity by increasing the proportion of erythroid colony-forming cells (BFU-e) in cell cycle as determined by 'thymidine suicide' experiments. The substitution of dialyzed fetal calf serum in the culture medium markedly inhibited the erythroid colony stimulation by ouabain. The deficient factor in dialyzed fetal calf serum appears to be K+, because the stimulatory influence of ouabain was restored upon reconstitution of the serum with K+. These studies suggest that ouabain-induced erythropoietic enhancement may involve mechanisms other than inhibition of membrane-bound Na+/K+ATPase.

中文翻译：

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体外促红细胞生成。IV。哇巴因对红系干细胞（CFU-e和BFU-e）的影响。

最近使用各种离子载体和强心苷的研究发现，从正常小鼠骨髓培养的晚期红系祖细胞（CFU-e）数量增加。我们报道强心苷哇巴因不仅增加了类红细胞祖细胞的数量，而且还增加了最早的类红细胞集落形成细胞（BFU-e）的数量。红血球干细胞数量的增加与剂量有关，在10（-15）M哇巴因时红血球菌落的数量最大增加。此外，哇巴因通过“自杀性胸腺嘧啶核苷”实验确定的细胞周期中红细胞集落形成细胞（BFU-e）的比例增加而发挥其刺激活性。在培养基中透析的胎牛血清的替代显着抑制了哇巴因对红系集落的刺激。透析过的胎牛血清中的缺陷因子似乎是K +，因为哇巴因在用K +重建血清后恢复了刺激作用。这些研究表明，哇巴因诱导的促红细胞生成可能涉及抑制膜结合的Na + / K + ATPase以外的其他机制。