Koeller D, DeSimone J, Heller P
Blood Cells. 1982;8(1):187-91.
The synthesis of Hb F in baboons after erythropoietic stress is markedly increased. The mechanism of this "reverse switch" is unknown, but erythropoietin is not directly responsible for it. Since D-thyroxine has been reported to cause Hb F increases in marmosets, we determined its effect in normal and anemic baboons whose erythropoiesis, hemoglobin fractions and regulation of hemoglobin synthesis are similar to those of man. No effect was demonstrated in the normal baboons. In the anemic animal the Hb F level did not increase beyond the elevation attributable to the erythropoietic stress itself. It is therefore, unlikely that D-thyroxine will increase Hb F levels in man.
红细胞生成应激后狒狒体内Hb F的合成显著增加。这种“反向开关”的机制尚不清楚,但促红细胞生成素并非直接原因。由于据报道D-甲状腺素可使狨猴的Hb F增加,我们测定了其对正常和贫血狒狒的影响,这些狒狒的红细胞生成、血红蛋白组分以及血红蛋白合成的调节与人相似。在正常狒狒中未显示出效果。在贫血动物中,Hb F水平并未超过因红细胞生成应激本身所致的升高。因此,D-甲状腺素不太可能使人的Hb F水平升高。