Abstract
SINCE the original hypothesis in 1893 by Miescher, 1 it has been generally accepted that the stimulus for the production of red blood cells by the bone marrow is anoxia. That anoxic anoxia stimulates erythropoiesis is well known from the observations of polycythemia and marrow hyperplasia at high altitudes and in various pathologic conditions producing decreased arterial oxygen tensions. Polycythemia produced by anemic anoxia and by cobalt have been explained by assuming local bone marrow anoxia and interference with bone marrow respiratory enzymes, respectively. However, direct studies of bone marrow oxygen tension have failed to show marrow anoxia after slow bleeding sufficient to produce an excellent erythropoietic response 2 or in chronic anemia. 3
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