1. The effect produced by the intravenous administration of collargol on the bone marrow of rabbits varies directly with the amount of collargol injected, and three fairly well defined stages could be recognized.

(a) An initial stage after comparatively few and small doses, with erythrocytic and endothelial hyperplasia in the bone marrow and with evidences of this stimulation in the peripheral blood in the form of young erythrocytes and normoblasts.

(b) An intermediary stage which followed the injection of larger amounts of collargol, and which was characterized by a predominant myeloid hyperplasia.

(c) A final stage with marked bone marrow aplasia and with colloidal silver deposited in endothelial cells, as well as in clasmatocytes. This was associated with a high grade anemia with low color index, resembling aplastic anemia in its main features. This stage terminated fatally.

2. There was no evidence of injury to blood cells in the peripheral circulation. The erythrocytic bone marrow aplasia was present before any appreciable decrease of red blood cells was found in the peripheral blood.

3. The results were less clear-cut in a series of rats, but anemia of a similar type was produced in all animals when sufficiently large doses were injected.

4. Splenectomy did not alter the course in rats materially.

5. It is fair to conclude that the cause of the anemia produced may be sought in the deviation of the parental endothelial cell toward clasmatocyte formation at the expense of the development of erythrocytes.

6. It is suggested that the results may be offered in support of the theory of the endothelial origin of both clasmatocytes and red blood cells.

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