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炎症性贫血的发病机制研究:红细胞生成受损的机制

Studies of the pathogenesis of anemia of inflammation: mechanism of impaired erythropoiesis.

作者信息

Weiss D J, Krehbiel J D, Lund J E

出版信息

Am J Vet Res. 1983 Oct;44(10):1832-5.

PMID:6638643
Abstract

Cats with induced sterile abscesses developed a hematologic disorder consistent with anemia of inflammation. Serum iron concentrations decreased while the abscess was present, but erythropoietin concentrations did not change significantly. Cobalt administration to control (healthy) cats resulted in polycythemia, reticulocytosis, and hyperferremia. Cats with abscesses responded to cobalt similarly; however, magnitudes of the polycythemia and reticulocytosis were less. Constant infusion of ferric citrate (IV) into cats with sterile abscesses maintained serum iron concentration in the normal to high range. The iron infusion did not prevent the anemia, but did enable the bone marrow to respond to the anemia.

摘要

患有诱导性无菌脓肿的猫出现了一种与炎症性贫血相符的血液学紊乱。在脓肿存在期间血清铁浓度下降,但促红细胞生成素浓度没有显著变化。给对照(健康)猫施用钴导致红细胞增多症、网织红细胞增多症和高铁血症。患有脓肿的猫对钴的反应类似;然而,红细胞增多症和网织红细胞增多症的程度较轻。向患有无菌脓肿的猫持续静脉输注柠檬酸铁可使血清铁浓度维持在正常至高范围。铁输注并不能预防贫血,但能使骨髓对贫血作出反应。

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