Two hematologically normal patients with glioblastoma and six patients with chronic lymphocytic leukemia received continuous 3H-thymidine infusions for 3--10 days. In autoradiographs of blood cell smears taken for 25 days or more after the beginning of 3H-thymidine administration the labeling index and the labeling intensity of granulocytes were determined. A sufficiently high labeling intensity, i.e. a sufficiently long autoradiographic exposure time was found to be critical for obtaining valid and reproducible results. On the basis of certain assumptions discussed in detail, complete labeling of cells with 3H-thymidine followed by autoradiographic evaluation and mathematical analysis of the labeling patterns seems to be a suitable method for estimation of kinetic parameters of postmitotic granulocytes in vivo. The mean intramedullary maturation and storage time was observed to be 115 +/- 7 h or neutrophils, 103 +/- 4 h for eosinophils and 103 +/- 11 h for basophils. The mean relative inflow rate into the blood (or relative turnover rate in the blood) was found to be 4.2 +/- 0.4/h for neutrophils, 4.0 +/- 0.4%/h for eosinophils and 1.2 +/- 0.3%/h for basophils. The mean blood transit time (or blood sojourn time) was estimated to be 25 +/- 2 h or neutrophils, 26 +/- 3 h for eosinophils and 89 +/- 21 h for basophils. Accordingly the half lifes (T 1/2) of granulocytes in the blood were 17.3 +/- 1.4 h for neutrophils, 18.0 +/- 2.1 for eosinophils and 62 +/- 15 h for basophils. Under the quasi steady state conditions of this study the kinetics of granulocytes in the present CLL patients appeared to be normal, despite a marked lymphocytic infiltration of the bone marrow. The apparent discrepancy between these findings and the data obtained with autotransfusion of DFP-labeled granulocytes is discussed.
The granulocyte cell renewal system of the dog is represented by a mathematical model consisting of the following compartments: The pool of pluripotential stem cells, the committed stem cell pool, divided into a blood and a bone marrow compartment, the proliferation pool, the maturation pool, the reserve pool and the blood pool of functional granulocytes. This chain of compartments is described by a system of non-linear differential equations. Cell losses anyplace in the system provoke increased production in all pools containing cells capable to divide. A reduced number of granulocytes in the blood pool stimulates production of a "granulocyte releasing factor" which mobilizes a rising number of cells to transit from the marrow reserve into the blood pool. The model was simulated on a digital computer. It was found to be capable to reproduce the steady state conditions and it also fits the data of two distinct experimental perturbations of the system both equally well. These perturbations are a loss of proliferating cells as it occurs after the administration of cytostatic drugs and losses of functional cells as they are induced by leukapheresis experiments of differing leukapheresis rates.
The effects of single-dose total-body X irradiation (TBI) on the granulocyte/macrophage progenitor cell (GM-CFC) population in bone marrow and blood of dogs were studied for dose levels of 0.78 and 1.57 Gy up to 164 days after irradiation. The blood GM-CFC concentration per milliliter was depressed in the first 7 days in a dose-dependent fashion to 5-16% of normal after 0.78 Gy and to between 0.7 and 5% after 1.57 Gy. The bone marrow GM-CFC concentration per 10(5) mononuclear cells, on the other hand, was initially reduced to about 45% of the average pre-irradiation value after 0.78 Gy and to 23% after 1.57 Gy. The regeneration within the first 30 to 40 days after TBI of the blood granulocyte values and the repopulation of the bone marrow GM-CFC compartment was associated with both a dose-dependent increase in the S-phase fraction of the bone marrow GM-CFC and a dose-dependent increase in colony-stimulating activity (CSA) in the serum. The slow repopulation of circulating blood GM-CFC to about only 50% of normal even between days 157 and 164 after TBI could be related to a correspondingly delayed reconstitution of the mobilizable GM-CFC subpopulation in the bone marrow.
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