Borch-Iohnsen B, Myhre K, Norheim G
Institute for Nutrition Research, University of Oslo, Norway.
Eur J Haematol. 1990 Jan;44(1):56-62. doi: 10.1111/j.1600-0609.1990.tb00348.x.
Iron-related changes in peripheral blood and variations in liver and spleen iron concentrations during alternating periods of hypoxia and normoxia have been investigated in iron-supplemented mice by chemical and histological methods. During hypoxia, packed cell volume increased from 40 to 70%. The iron content of the liver increased during the first hypoxic and the following normoxic period, while an increase in spleen iron started after the first hypoxic period. Transferrin saturation fell from about 60 to about 20% during hypoxia and normalized during normoxia. Hypoxia together with iron supplementation led to increased erythropoiesis and parenchymal iron deposition in liver. The reduction in transferrin saturation may be attributed to the effective uptake of iron by hepatocytes simultaneously with the erythropoiesis. The spleen seemed to participate in the production of red cells during hypoxia. The increase in spleen iron during normoxia can be explained by the role of the spleen in the catabolism of excess erythrocytes.
通过化学和组织学方法，对补充铁的小鼠在缺氧和常氧交替期间外周血中铁相关变化以及肝脏和脾脏铁浓度的变化进行了研究。在缺氧期间，红细胞压积从40%增加到70%。肝脏铁含量在第一个缺氧期和随后的常氧期增加，而脾脏铁的增加在第一个缺氧期后开始。缺氧期间转铁蛋白饱和度从约60%降至约20%，常氧期间恢复正常。缺氧加上补充铁导致肝脏红细胞生成增加和实质铁沉积。转铁蛋白饱和度的降低可能归因于肝细胞在红细胞生成同时有效摄取铁。脾脏似乎在缺氧期间参与红细胞的产生。常氧期间脾脏铁的增加可以通过脾脏在多余红细胞分解代谢中的作用来解释。
