Dunn C D, Smith L N, Leonard J I, Andrews R B, Lange R D
Exp Hematol. 1980;8 Suppl 8:259-82.
During chronic hypoxia, the number of splenic erythroid progenitor cells in mice, particularly CFU-E, increased dramatically but transiently. Since all three classes of erythroid progenitors in the femoral bone marrow were suppressed, a large part of this increase might be attributed to migration of CFU-E and/or their progenitors from the medullary cavity. The changes in CFU-E were preceded 48-72 hours earlier by an increase in serum erythropoietin (Ep) titers which, in turn, had been preceded by a rapid and marked "shift-to-the-right" in the hemoglobin oxygen dissociation curve. During hypoxia, the mice lost a considerable fraction of their body weight. Computer simulations, using a mathematical model of erythropoietic regulation, suggest that this weight loss, either indirectly by reducing the need for red cells in a smaller-than-control animal or by directly altering the sensitivity of the Ep-producing mechanism, is the major cause of the falling Ep titers despite continuation of the hypoxic stress. Because of high endogenous 59Fe incorporation levels, it was not possible to confirm the thesis that animals with an expanded Erythropoietin Responsive Cell (ERC) compartment would be more sensitive to exogenous erythropoietin than are mice with a normal or reduced ERC population.
在慢性缺氧期间，小鼠脾脏红系祖细胞的数量，尤其是集落形成单位 - 红细胞（CFU - E），显著但短暂地增加。由于股骨骨髓中的所有三类红系祖细胞均受到抑制，这种增加的很大一部分可能归因于CFU - E及其祖细胞从骨髓腔的迁移。CFU - E的变化在48 - 72小时之前，血清促红细胞生成素（Ep）滴度增加，而血清促红细胞生成素滴度增加又先于血红蛋白氧解离曲线快速且显著的“右移”。在缺氧期间，小鼠体重减轻了相当一部分。使用红细胞生成调节数学模型进行的计算机模拟表明，这种体重减轻，要么是通过间接减少较小体型动物对红细胞的需求，要么是通过直接改变促红细胞生成素产生机制的敏感性，是尽管缺氧应激持续但促红细胞生成素滴度下降的主要原因。由于内源性59Fe掺入水平较高，无法证实红细胞生成素反应性细胞（ERC）区室扩大的动物比正常或减少ERC群体的小鼠对外源促红细胞生成素更敏感这一论点。
