We evaluated the possibility of hemopoiesis stimulation with hyaluronidase. The response of the blood system depended on the dose of this enzyme. Functional activity of hemopoietic precursor cells increased under the influence of hyaluronidase in a dose of 20 arb. units, which was accompanied by an increase in the secretion of hemopoietins by adherent myelokaryocytes and elevation of hemopoietic activity in blood plasma. The number of erythrokaryocytes and mature neutrophilic granulocytes in the bone marrow, as well as the count of reticulocytes and neutrophils in the peripheral blood increased under these conditions. Administration of hyaluronidase in a high dose (100 arb. units) led to uncoupling of proliferation and differentiation of hemopoietic precursors and produced no considerably changes in the blood.

Morphological composition of the bone marrow, content of hemopoietic precursors, intensity of their proliferation and differentiation, and the size of mesenchymal precursor pool were studied in experiments on CBA/CaLac mice with myelosuppression induced by adriamycin, cyclophosphamide, or 5-fluorouracil in the maximum tolerated doses. The dynamics of changes in the content of granulomonocyte precursors in the bone marrow after cytostatic treatment was similar to that of erythroid precursors. Changes in the content of stromal mechanocytes were specific for each cytostatic. Different character of the reaction of the hemopoietic and mesenchymal stem cells to the test cytostatics was demonstrated.

We studied the reactions of granulocytic hemopoietic stem after acute hypoxia and during the development of posthypoxic encephalopathy. Damage to brain structures was associated with intensification of the bone marrow hemopoiesis due to activation of hemopoiesis-inducing microenvironment and more intense formation of hemopoietic islets, despite reduced proliferative capacity of granulocytic precursors.

The effects of dimethylsulfoxide on the state of mesenchymal precursors in vivo were demonstrated. Treatment with dimethylsulfoxide reduced the content of stromal clonogenic elements in the bone marrow and inhibited mobilization of mesenchymal precursors induced by granulocyte colony-stimulating factor. In in vitro system, dimethylsulfoxide inhibited proliferation of fibroblast, erythroid, and granulomonocytic colony-forming units and stimulates maturation of hemopoietic precursors.

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