The effect of anemic anoxia on the cellular development of nucleated red cells.
نویسنده
چکیده
With the technical assistance of Elva Ruiz A NUMBER of distinct functional stages can be recognized in the development of noiidifferentiated stem cells to mature red blood cells. Several investigators have attempted to design a model of this process based on studies of bone marrow morphology,”2 metabolism,1 mitotic activity4’5 and volumetric changes of the nuclei. 7 From these studies emerge a rough but useful outline of red cell development ( see figure 1). Stage I ( fig. 1 ) represents the period in which an undifferentiated but multipotential stem cell is differentiated into an immature red cell, the pronormoblast. It appears that this process must involve a division where one of the resulting cells is differentiated into a pronormoblast while the other remains undifferentiated, thus preventing a depletion of multipotential stem cells. Stage II ( fig. 1 ) represents the period in which maturation and hemoglobin synthesis take place concomitantly with mitotic division. The exact number of divisions is unknown, but on the basis of bone marrow differential counts, three divisions during Stage II would appear to be a reasonable assumption. At the end of this stage the red cell nucleus has become pyknotic and )robably incapable of further divisions. Stage III ( fig. 1 ) represents the period in which the final maturation of the cytOl)lasm takes place with disappearance of mitochondria and ribose nucleic acid. The pyknotic nucleus is extruded and despite suggestions by \Veicker7 that amitotic division might occur, it appears unlikely that further multiplicati()n takes place. it is assumed that the maturation and division of red cell precursors will go through these stages in an orderly manner if the necessary enzymes, hormones and metabolic building blocks are available. Under such conditions the rate of red cell production appears to be regulated solely by a feedback mechanism which balances the demand for oxygen in the tissues wjth the production of oxygen-carrying hemoglobin.8 Although the dynamics of this regulatory mechanism are poorly understood, recent experimental evidence strongly supports the concept that an anoxic stimulus is generated in a specific, probably extramedullary site and transmitted by means of a humoral erythropoietic factor or erythropoietine to the bone marrow.9 This device is capable of maintaining a stable hemoglobin concentration and is triggered by minute changes in the supply of
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ورودعنوان ژورنال:
- Blood
دوره 14 4 شماره
صفحات -
تاریخ انتشار 1959