Do you know about - Detailed Histology of Erythrocytes (Red Blood Cell Formation)
Hemoglobin! Again, for I know. Ready to share new things that are useful. You and your friends.The erythrocyte is formed from the hemocytoblast in the red bone marrow. The hemocytoblast forms the pro-erythroblast, The initial cell of this series has a deep blue (basophilic) staining cytoplasm and therefore is called a basophilic erythroblast. The chief turn in the erythroblast is accumulation of hemoglobin in the cytoplasm. As the basophilic material decreases and the number of hemoglobin increases, the cell is called a polychromatic erythroblast, which describes its combination of staining properties. At the same time as the nucleus is decreasing in size, the basophilic material disappears, so that the cell is uniformly stain by eosin dye, hence the name orthochromatic erythroblast, or normoblast, finally the normoblast fully loses its nucleus by a process of extrusion as it squeezes straight through the pores of the membrane into the capillary. As a effect of losing its nucleus, the cell caves on both sides, giving the mature erythrocyte its characteristic appearance as a biconcave disc. While each of these stages the different cells continue to endure mitosis so that increasingly greater numbers of cells are produced.
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We had a good read. For the benefit of yourself. Be sure to read to the end. I want you to get good knowledge from Hemoglobin.Normally some of the circulating erythrocytes, called reticulocytes, hold a small number of basophilic reticulum. Commonly the total proportion of circulating reticulocytes (known as the reticulocyte count) is between 0.5% and 1.5%. A turn in the number of reticulocytes is an indicator of increased red blood cell production or hyper-functioning of the bone marrow. The reticulocyte count is a simple laboratory test frequently used to indirectly analyze hemopoiesis.
Regulation of erythrocyte production
The usual life span of the mature erythrocyte is 120 days. Apparently as red blood cells grow old, their membranes come to be fragile and at last mature. The contents of the cell fragment as they circulate straight through the blood vessels and are phagocytized by the reticuloendothelial cells in the spleen, liver, and bone marrow. The hemoglobin is broken down into the iron-containing pigment hemosiderin and the bile pigments biliverdin and bilirubin. Most of the iron is reused by the bone marrow for production of new red blood cells or stored in the liver and other tissues for time to come use. The bile pigments are excreted by the liver in bile.
Normally there is a homeostatic equilibrium between the regulation of red blood cell production and destruction. This equilibrium ensures sufficient tissue oxygenation and a blood viscosity that allows the blood to flow freely straight through the vessels. The basic regulator of erythrocyte production is believed to be tissue oxygenation. In states of tissue hypoxia, erythropoietin (also called erythropoietic stimulating factor or hemopoietin) is released by the kidneys into the blood stream. As a result, the bone marrow is stimulated to furnish new red blood cells. The major activity seems to be an growth in both the maturation rate and mitosis of all stages of erythrocyte production, but primarily at the stem cell level.
During this rapid growth of red blood cell production, the circulating erythrocytes may not be totally matured. Consequently, the number of reticulocytes may growth dramatically (as high as 30% or more of the total red blood cell count). Even normoblasts may appear in the blood. Failure to search for this rise in erythrocyte and reticulocyte count is an indicator of bone marrow failure.
Once tissue oxygenation is adequate, the production of erythropoietin ceases. Thus, tissue oxygen requirements control both the stimulation and termination of erythrocyte production. It is foremost to note that it is the function of red blood cells to transport oxygen to the tissues in response to their needs, not the circulating numbers of erythrocytes that is the basic regulatory mechanism. This explains why polycythemia (increase in the number of erythrocytes) occurs in conditions of prolonged tissue hypoxia, such as cyanotic heart defects. If the circulating numbers of erythrocytes controlled erythropoietin release, this feedback mechanism would control erythrocyte production at a constant level (4.5 to 5.5 million/mm3 of blood) regardless of exiting tissue hypoxia.
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