Red Blood Cell Formation
The term erythropoiesis (erythro = RBC, and poiesis = to make) is used to describe the process of RBC formation or production. In humans, erythropoiesis occurs almost exclusively in the red bone marrow. (The yellow bone marrow is primarily composed of fat, but, in response to a greater need for RBC production, the yellow bone marrow can turn to red marrow.) The red bone marrow of essentially all bones produces RBCs from birth to about five years of age. Between the ages of 5 to 20, the long bones slowly lose their ability to produce RBCs. Above age 20, most RBCs are produced primarily in the marrow of the vertebrae, the sternum, the ribs, and the pelvis. Let's examine how RBCs are produced and, ultimately, how they are destroyed. The organ responsible for "turning on the faucet" of RBC production is the kidney (Figure 4). The kidneys can detect low levels of oxygen in the blood. When this happens, the kidneys respond by releasing a hormone called erythropoietin, which then travels to the red bone marrow to stimulate the marrow to begin RBC production.
Now, once the erythropoietin stimulates the red bone marrow to begin manufacturing RBCs, a series of events occurs. In the bone marrow there are many special stem cells from which RBCs can be formed. As these cells mature, they extrude their nucleus as they slowly fill with hemoglobin until they are bright red reticulocytes ready to escape the bone marrow and squeeze into the blood capillaries to begin circulating around the body. In a blood sample, the reticulocytes can be distinguished from RBCs because they still contain some speckles or pieces of their nucleus. Within a few days, this reticulocyte completely loses all its nuclear material and becomes a full-fledged RBC that is ready to serve the oxygen needs of the body. After about three to four months, the RBC has worked so hard that it begins to weaken. The membranes of old RBCs become very fragile and the cells may rupture during passage through some tight spots in the circulation. These old and damaged RBCs are "eaten" primarily by the Spleen, and most of the leftover components (especially the iron from the hemoglobin) are recycled to form new RBCs.
The production of new RBCs occurs as the need arises. A natural need always exists to produce new RBCs to replace the ones that have gotten old, or have been damaged, and have "died." Old RBCs die every day in our bodies and more new ones are also born every day. The body can also increase production of RBCs in response to special needs. As mentioned previously, new RBCs must be produced when a person enters a high altitude environment. At very high altitudes, where the quantity of oxygen in the air is greatly decreased, insufficient oxygen is transported to the tissues, and red cells are produced so rapidly that their number in the blood is considerably increased. Therefore, it is obvious that it is not the concentration of RBC's that controls the rate of red cell production, but instead, it is the functional ability of the RBCs to transport oxygen to the tissues in response to the tissue demand for oxygen that controls the rate of RBC production. In other words, it's just like the economic concept of "supply and demand." If the supply of oxygen is LESS than what the body demands, the MORE RBCs are produced. If the supply of oxygen is MORE than what the body demands, the FEWER RBCs are produced. This wonderful negative feedback mechanism works fine on Earth. How about in space?
The RBC lifetime is about 120 days.
a) Kidneys respond to a lower than normal oxygen concentration in the blood by releasing the hormone erythropoietin.
b) Erythropoietin travels to the red bone marrow and stimulates an increase in the production of red blood cells (RBCs).
c) The red bone marrow manufactures RBCs from stem cells that live inside the marrow.
d) RBCs squeeze through blood vessel membranes to enter the circulation.
e) The heart and lungs work to supply continuous movement and oxygenation of RBCs.
f) Damaged or old RBCs are destroyed primarily by the Spleen.
Term first found in HGS Manual: Page 49