Dunn C D, Jarvis J H, Napier J A
Exp Hematol. 1976 Nov;4(6):365-81.
During hypoxia, elevated ESF levels occur which are accompanied by increased erythropoietic activity resulting in progressive elevation of the haemoglobin and haematocrit concentration. An attempt has been made to correlate ultrastructural changes in the kidney with changes in serum ESF concentrations and the erythropoietic state of mice exposed to continuous hypoxia for 3 weeks. A series of changes in the epitheloid and proximal tubules cells occurred which may be related to the biogenesis of erythropoietin. However, no detectable ESF or renal erythropoietic factor could be extracted from the kidneys at the time of maximal ultrastructural changes. Although some ESF-inhibitory material was demonstrated, it could not be extracted into lipid solvents. It is suggested that the failure to consistently extract an erythropoietic factor from the kidneys of hypoxic mice may be related to the absence of renal storage at the onset of increased peripheral demand. Other levels and durations of hypoxia may help to elucidate the role of the kidneys in regulating serum ESF levels.
在缺氧期间，促红细胞生成素（ESF）水平升高，同时红细胞生成活性增强，导致血红蛋白和血细胞比容浓度逐渐升高。已尝试将肾脏的超微结构变化与血清ESF浓度变化以及连续缺氧3周的小鼠的红细胞生成状态相关联。上皮样细胞和近端肾小管细胞发生了一系列变化，这可能与促红细胞生成素的生物合成有关。然而，在超微结构变化最大时，无法从肾脏中提取出可检测到的ESF或肾红细胞生成因子。虽然证明了一些ESF抑制物质，但它不能被提取到脂质溶剂中。有人认为，未能从缺氧小鼠的肾脏中持续提取红细胞生成因子可能与外周需求增加开始时肾脏中缺乏储存有关。其他缺氧水平和持续时间可能有助于阐明肾脏在调节血清ESF水平中的作用。
