Gordon A S, Naughton B A
Exp Hematol. 1980;8 Suppl 8:14-28.
Evidence is presented for production, by the subtotally hepatectomized (hepx) rat, of a factor which induces morphological and physiological hyperactivity of the Kupffer (K) cells and increased formation of Ep by the regenerating liver. This factor, originally termed hepatopoietin (Hp), and more recently the hepatic erythropoietic factor (HEF), is detectable in higher concentration in the hepatic venous blood than in blood draining other organs, thus supporting its hepatic origin. Production of the HEF is best related to hyperactivity of the K cells and not to the parenchymal (P) cells. The HEF can be demonstrated by administering serum from hepx donors to normal rats which respond with increased production of Ep when nephrectomized (nephrx) and rendered hypoxic. Removal of the kidneys from hepx donors further augments the Ep response to this serum in recipients. Subtotal hepx also evokes the production of a renal inhibitory factor (RIF) which reduces the ability of the liver to function as an extrarenal source of Ep. This inhibitor is found in renal venous blood and not in blood draining other organs. It is suggested that the RIF reduces the hepatic Ep response to hypoxia by diminishing the production and/or activity of the HEF. The RIF possesses no anti-Ep activity and its appearance and actions are not influenced by accumulation of metabolic wastes (as in the nephrx or ureterally-ligated rat). Erythroblastic nests have been observed in regenerating livers at 24-48 hr after subtotal hepx. It would seem that removal of a considerable part of the liver, which stimulates hepatic regeneration, confers upon this organ an increased ability to produce Ep and to function as a hematopoietic inductive microenvironment (HIM) for erythropoiesis.
有证据表明，部分肝切除的大鼠可产生一种因子，该因子可诱导库普弗细胞发生形态和生理上的过度活跃，并使再生肝脏中促红细胞生成素（Ep）的生成增加。这种因子最初被称为肝细胞生成素（Hp），最近被称为肝源性促红细胞生成因子（HEF），在肝静脉血中的浓度高于引流其他器官的血液，这支持了其肝脏来源。HEF的产生与库普弗细胞的过度活跃最相关，而与实质细胞无关。通过将部分肝切除供体的血清给予正常大鼠来证明HEF的存在，当这些正常大鼠被切除肾脏并处于低氧状态时，它们对血清的反应是Ep生成增加。从部分肝切除供体中摘除肾脏会进一步增强受体对这种血清的Ep反应。部分肝切除还会引发肾抑制因子（RIF）的产生，该因子会降低肝脏作为肾外Ep来源的功能能力。这种抑制剂存在于肾静脉血中，而不存在于引流其他器官的血液中。有人认为，RIF通过减少HEF的产生和/或活性来降低肝脏对低氧的Ep反应。RIF不具有抗Ep活性，其出现和作用不受代谢废物积累（如在切除肾脏或输尿管结扎的大鼠中）的影响。在部分肝切除后24 - 48小时的再生肝脏中观察到了红系造血岛。似乎切除相当一部分肝脏（这会刺激肝脏再生）赋予了这个器官增加的产生Ep的能力，并使其能够作为红细胞生成的造血诱导微环境（HIM）发挥作用。
