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To elucidate mechanisms underlying the prolonged monocytopenia induced in the peripheral blood of mice by injection of a subcutaneous depot of hydrocortisone acetate, the effect of this compound on the production of monocytes and their release from the bone marrow was studied. Hydrocortisone was found to cause a rapid reduction of the bone marrow promonocytes to about 65% of their initial number. The number of monocytes in the bone marrow decreased gradually, over a period of 96 h, to 75% of the initial value. The mitotic activity of the promonocytes was not diminished, as judged from the labeling in vitro with [(3)H]thymidine and the DNA-synthesis and cell-cycle times of these cells. The production of monocytes was only moderately diminished, i.e., to about 80% of the normal amount. The release of monocytes from the bone marrow was found to be influenced by hydrocortisone. After in vivo labeling with [(3)H]thymidine the monocyte-labeling indices were initially significantly higher in hydrocortisone-treated than in normal mice. It is concluded that a decreased production of monocytes in the bone marrow cannot account for the prolonged monocytopenia in the peripheral blood after hydrocortisone administration. However, hydrocortisone interferes with the release of newly formed monocytes from the bone marrow, resulting in a prolonged sojourn of these cells in this compartment.

THE EFFECT OF GLUCOCORTICOSTEROIDS ON THE PROLIFERATION AND KINETICS OF PROMONOCYTES AND MONOCYTES OF THE BONE MARROW