Mechanism of Cobalt Polycythemia. Effect of Ascorbic Acid

Abstract

Waltner and Waltner 1 discovered that cobalt when given to animals produced a polycythemia as shown by the increase in the number of red cells and in hemoglobin. Mascherpa 2 from studies of cobalt polycythemia on dogs reported an increased activity of the bone marrow. For experiments on the mechanism of this polycythemia rabbits were used so that blood could be withdrawn in sufficient quantities to measure the hemoglobin concentration and count the red cells simultaneously. By daily subcutaneous injection of 0.01 gm, CoSO₄ a definite polycythemia was produced within 6 or 7 days, accompanied by the appearance in the circulating blood of reticulocytes and erythroblasts. The presence of these young cells was strikingly manifested by the increased respiration of red cells from animals with cobalt polycythemia, an increase which fails to appear in human polycythemia vera (Table I). The increase in respiration was about 10 times as great when erythroblasts were present.

The addition of CoSO₄ (0.01 mg.) in vitro to the red cell suspensions from cobalt polycythemia was followed by a marked inhibition in respiration as contrasted with the lack of such effect in the red cells of normal rabbits. This inhibition was practically confined to the respiration of immature red cells, being greater in the bone marrow than in the spleen and kidney (Table II).

The findings of Berwald, Arsenau, and Dooley 3 that cobalt fails to produce polycythemia in splenectomized rats did not hold in the case of rabbits, a discrepancy which may be explained by the fact that splenectomized rats develop an anemia by B. muris.

Ascorbic acid seems to assist in the maintenance of a determined level of red cells in the circulating blood, this effect in certain cases of anemia having been reported many times.