Naughton B A, Dornfest B S, Preti R A, Johnson R, Gordon A S
J Med. 1984;15(1):45-58.
Hypoxia stimulates erythropoietin (Ep) production and subsequent stimulation of erythropoiesis. Chronically applied hypoxia results in a variety of physiological alterations including polycythemia, hemoglobinemia, and vascular and metabolic changes. As red cell mass increases to such an extent to allow for adequate tissue oxygenation, plasma Ep levels drop and the rate of erythropoiesis is lowered. In the present work, the precise contribution of the kidney and the liver to the Ep response to acutely administered hypoxia (6-24 hr/0.4 atm) was determined using an in situ tandem perfusion of the liver and kidneys. The results indicate that hepatic and renal Ep production during different intervals of acute hypoxia is not uniform. This alteration may be partially explained by the reported reduction in splanchnic blood flow and a possible redistribution of hepatic microcirculation, which may cause the liver to become more hypoxic than the kidney under the same ambient pO2. The role of the liver becomes more pronounced as the time of acute hypoxic exposure increases, whereas the Ep content of renal perfusates is not drastically altered. At certain intervals during hypoxia, the liver displays a greater potential to elaborate Ep.
缺氧刺激促红细胞生成素（Ep）的产生，随后刺激红细胞生成。长期应用缺氧会导致多种生理改变，包括红细胞增多症、血红蛋白血症以及血管和代谢变化。随着红细胞量增加到足以实现充分的组织氧合，血浆Ep水平下降，红细胞生成速率降低。在本研究中，通过肝脏和肾脏的原位串联灌注，确定了肾脏和肝脏对急性给予缺氧（6 - 24小时/0.4个大气压）时Ep反应的确切贡献。结果表明，急性缺氧不同时间段内肝脏和肾脏的Ep产生并不均匀。这种改变可能部分是由于所报道的内脏血流量减少以及肝脏微循环可能的重新分布，这可能导致在相同环境pO2下肝脏比肾脏更缺氧。随着急性缺氧暴露时间增加，肝脏的作用变得更加显著，而肾脏灌注液中的Ep含量没有明显改变。在缺氧期间的某些时间段，肝脏表现出更大的产生Ep的潜力。
