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Z Rolovic, N Basara, N Stojanovic, N Suvajdzic and V Pavlovic-Kentera
Medical Faculty of Belgrade University, Yugoslavia.
The Belgrade laboratory (b/b) rat has a hereditary hypochromic microcytic
anemia because of defective transmembrane iron transport into
erythroblasts. The present study was prompted by our previous work in which
we showed that the b/b rat has hypomegakaryocytic thrombocytopenia
associated with increased megakaryocyte size. To define the basic mechanism
underlying this abnormality in the b/b rat we have studied both
megakaryocytopoiesis and granulopoiesis in anemic b/b rats, chronically
transfused b/b rats, iron-treated b/b rats, and controls. We have found
decreased concentrations of megakaryocyte and granulocyte progenitors in
the marrow of b/b rats. Full correction of the severe anemia by chronic
transfusion resulted in normalization of megakaryocyte progenitors, small
acetylcholinesterase positive cells, megakaryocyte size, and platelet
counts, along with granulocyte progenitors. In contrast, the partial
correction of anemia obtained by iron treatment resulted in improvement,
but not normalization, of these parameters. These findings indicate that
abnormal megakaryocytopoiesis in the b/b rat can be best interpreted as a
consequence of hypoxia because of the severe anemia. Because we have
recently shown that the number of erythroid progenitors in b/b rats is also
low, we propose that abnormal megakaryocytopoiesis in this animal is a
reflection of an acquired stem cell disorder induced by the prolonged
hypoxia resulting from the severe anemia.
This article has been cited by other articles:
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| Copyright © 1991 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||