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.

Brain pathology (acute hypoxia and posthypoxic encephalopathy) is associated with less pronounced hyperplasia of the bone marrow erythroid stem (due to decreased count of proliferating committed precursors) and hemolytic anemia, while secretory activity of stromal cells of the hemopoiesis-inducing microenvironment is not impaired. Severe oxygen deficiency affects erythroid precursors and impairs production of functionally normal erythrocytes in the posthypoxic period.

The mechanisms of suppression and recovery of the bone marrow erythroid stem were studied on the model of myelosuppression induced by administration of carboplatin in the maximum tolerated dose. Single administration of the cytostatic led to the development of long-term hypoplasia of hemopoiesis. Despite enhanced proliferation of erythroid precursor caused by increased erythropoietic activity of blood plasma and bone marrow cells, inhibition of cell maturation prevented recovery of the content of morphologically recognizable erythrokaryocytes in the bone marrow.

We studied the state of different pools of mesenchymal precursor cells in the bone marrow, peripheral blood, and wound surface after modeling of tissue damage by skin flap removal. The participation of regional and circulating stromal precursors in the healing of skin defect and the absence of compensatory reaction of the regeneratory process deep reserve, mesenchymal stem cells of the bone marrow, was demonstrated.