Hepatic production of erythropoietin in a phenylhydrazine-induced compensated hemolytic state in the rat.

Abstract

The relative roles of the kidney and liver as a source of Ep in a fully compensated hemolytic state were investigated. A compensated hemolytic anemia was induced in rats by injections of PHZ over a 6-week period. Verification of a fully compensated hemolytic state was established by MCV, MCH, MCHC, BV, PV, CRCV, peripheral reticulocyte counts, and bone marrow counts. The kidneys and livers of the PHZ-injected rats were subjected to concurrent perfusion at weekly intervals over the treatment period and the perfusate assayed for Ep activity. The kidney was found to be the principal source of Ep during the earlier stages of the anemia and the liver became increasingly important as a source of Ep during the later stages as the anemia became progressively compensated. By the fifth and sixth weeks of treatment, when the anemia was fully compensated, the livers of the PHZ-treated rats were the principal source of Ep. During these last 2 weeks of treatment, the amount of Ep recovered from the renal effluents of PHZ-injected rats was no greater than that collected from the renal effluents of saline-injected rats. The data indicate that the liver is the primary, if not the only, source of the higher titers of Ep in the fully compensated hemolytic state induced in the rat by long-term PHZ treatment.

Cite this paper

@article{Dornfest1983HepaticPO, title={Hepatic production of erythropoietin in a phenylhydrazine-induced compensated hemolytic state in the rat.}, author={B S Dornfest and Brian A Naughton and Ron Johnson and A. S. Gordon}, journal={The Journal of laboratory and clinical medicine}, year={1983}, volume={102 2}, pages={274-85} }