Hematopoiesis(redirected from hematopoiesis depression)
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The process by which the cellular elements of the blood are formed. The three main types of cells are the red cells (erythrocytes), which serve to carry oxygen, the white cells (leukocytes), which function in the prevention of and recovery from disease, and the thrombocytes, which function in blood clotting. The formation of these cells is one of the most active and important processes in the body. Most of the circulating cells live only for a short time and must be replaced in order to maintain life. For instance, in the human adult a red blood cell has a life of 120 days; 250 billion new red cells have to be produced daily to replace those that are destroyed.
Blood cells originate in the reticuloendothelial tissue, which is a loose, fibrous, highly vascularized mesh of fibers, endothelial cells, and macrophages. Within the spaces of the tissue are found the precursor (blast) cells of the definitive adult types. For the sake of convenience, the reticuloendothelial tissue is divided into two general but imprecise types: lymphoid and myeloid tissue. Lymphoid tissue is primarily localized in the lymph nodes of the lymphatic system and is also in the spleen, thymus, and bone marrow. Several classes of white cells are produced, including the lymphocytes, macrophages, and monocytes. See Cellular immunology, Lymphatic system
Myeloid tissue is normally limited in humans to the red bone marrow of the ribs, sternum, vertebrae, and proximal ends of the long bones of the body. It is concerned with the production of the erythrocytes and certain types of leukocytes. The latter are the granular leukocytes (called eosinophils, basophils, and neutrophils on the basis of the affinity of granules in their cytoplasm for certain dyes) and megakaryocytes. Fragments of megakaryocytes form the blood platelets (thrombocytes), which are necessary for blood clotting. See Blood
the process by which blood cells form, develop, and mature in animals and man.
The blood’s formed elements are highly specialized cells with a short life cycle: about 120 days for human erythrocytes, about five days for leukocytes, from several days to several months for lymphocytes, and about four days for thrombocytes. Despite the continuous destruction of blood cells, the number of cells re-mains more or less constant throughout the life of the organism, since the dying cells are replaced by new ones. In invertebrates, hematopoiesis takes place mainly in the perivisceral fluids and in the blood itself. In adult mammals and man, it takes place in the hematopoietic organs: the erythrocytes, granular leukocytes, and thrombocytes in the bone marrow; lymphocytes in the lymph nodes, spleen, thymus, and bone marrow; and monocytes and macrophages, in the bone marrow. All mature blood cells, regardless of their differences, apparently originate from a single type of parental hematopoietic (stem) cell. The strain of these parental cells is maintained in the body for life, thus ensuring the continuity of hematopoiesis. Upon maturing (differentiating), the hematopoietic cells undergo complex changes and divide several times more. Therefore, a great many specialized formed elements develop from a small number of parental cells.
Hematopoiesis is controlled in a complex manner by changes in the quantity and quality of the blood cells according to the needs of the body (for example, when the amount of oxygen in the air changes). Cells are replenished when blood is lost. This regulation is accomplished by a number of hormones, vitamins (for example, cyanocobalamin, or B12; and folic acid, or Bc), and special substances, called erythropoietins, to which various stages of the hematopoietic process are sensitive. The mechanisms regulating the rate of reproduction and maturation of the individual categories of hematopoietic cells are still largely un-known.
In the embryos of all mammals, including man, hematopoiesis starts in the yolk sac, where the hematopoietic cells originate from mesenchymal cells. Foci of hematopoietic tissue form in the embryonic mesenchyma and, later, in the liver (where red and white blood cells are formed) and thymus (where lymphocytes are formed). Still later, hematopoiesis shifts to the bone marrow, and lymphocytes begin to develop in the thymus, spleen, and lymph nodes.
REFERENCESZavarzin, A. A. Izbr. tr., vol. 4: Ocherki evoliutsionnoi gistologii krovi i soedinitel’noi tkani. Moscow-Leningrad, 1953.
Fiziologiia sistemy krovi. Leningrad, 1968.
Chernigovskii, V. N., S. Iu. Shekhter, and A. laroshevskii. Reguliatsiia eritropoeza. Leningrad, 1967.
Eksperimental’nye issledovaniia mekhanizmov gemopoeza. Sverdlovsk, 1971. (Collection of articles.)
Hematopoietic Cellular Proliferation. Edited by F. Stohlman. New York, 1970.
Regulation of Hematopoiesis, vols. 1-2. Edited by A. S. Gordon. Appleton, 1970.
Depending on the nature of the damage to the hematopoietic organs, hematopoietic disorders are defined as hyperplastic (with the excessive formation of elements of hematopoietic tissue), on the one hand, and hypoplastic and aplastic, on the other (depression of hematopoiesis; interference with the division and, to a lesser degree, the maturation of hematopoietic cells). The cate-gory of the injured cells and the degree of maturity (weakly differentiated cells and elements of granulo-, erythro-, thrombocyto, and lympho-poiesis at various stages of maturity) are other factors that determine the nature of the diseases.
Hyperplastic hematopoiesis is most pronounced in leukemias and erythremia. In leukemias, cells of the bone marrow lose their capacity for differentiation (maturation), and their proliferation (multiplication) may be retarded. The life-span of these immature elements increases, so that a vast number of cells of various cellular lines and degrees of maturity accumulate in the hematopoietic organs and blood. This determines the form of the leukemia (acute, chronic, myelocytic, lymphocytic).
Karyological studies have revealed changes in the chromosomes of the hematopoietic cells in certain forms of leukemia, indicating that these hematopoietic disturbances have a heritary nature.
In hypoplasia and aplasia, it is either the hematopoietic stem cells or the earliest cellular forms of erythrocytopoiesis, granulocytopoiesis, and thrombocytopoiesis that are injured. These disturbances are manifested not only by a depletion of hematopoietic cells in the bone marrow but also by a de-crease in the number of red blood cells (and, consequently, in the amount of hemoglobin), white blood cells (granulocytes), and thrombocytes (hypoplastic and aplastic anemias, agranulocytoses, metastases of tumors to bone marrow). Hematopoietic disorders assume a peculiar character when the body is suffering from a deficiency of certain vitamins, trace elements, or enzymes. For example, a deficiency of vitamin B12 and folic acid impairs the normal formation of red blood cells, and cells characteristic of embryonic hematopoiesis in the liver appear in the bone marrow (B12 and folic acid deficiency anemias). If iron is deficient, the red blood cells have little hemoglobin and iron deficiency anemia develops, even though the total number of erythrocyte-forming cells in the bone marrow and erythrocytes in the blood may remain normal.
If the structure of hemoglobin is impaired (hemoglobinopathies) or if certain enzymes in the red blood cells are absent or deficient (enzymopathies), the red blood cells become abnormal and are quickly destroyed in the bloodstream or, more often, in the spleen (hemolytic anemias). In such cases, the bone marrow and peripheral blood contain a substantial amount of immature cells (normoblasts and reticulocytes) of the erythrocytic series.
Hematopoietic disorders involving mainly lymphopoiesis weaken immunity and cause certain protein changes in the blood. True hyperplastic hematopoiesis must be distinguished from its reactive states, called leukemoid reactions, which can be provoked by infections and intoxications. Eliminating the pri-mary causes of the reactive states brings about a normalization of hematopoiesis.
REFERENCESFainshtein, F. E. Aplasticheskie i gipoplasticheskie anemii. Moscow, 1965.
Kassirskii, I. A., and G. A. Alekseev. Klinicheskaia gematologiia, 4th ed. Moscow, 1970.
Policard, A., and M. Bessis. Elementy patologii kletki. Moscow, 1970. (Translated from French.)
A. M. POLIANSKAIA