A Test for Red Cell Production

1952 ◽  
Vol 7 (3) ◽  
pp. 129-143 ◽  
Author(s):  
Rex L. Huff ◽  
Cornelius A. Tobias ◽  
John H. Lawrence
Keyword(s):  
Red Cell ◽  
2014 ◽  
pp. 1-1
Author(s):  
Ramadas Nayak ◽  
Sharada Rai
Keyword(s):  
Red Cell ◽  

Blood ◽  
1976 ◽  
Vol 48 (4) ◽  
pp. 547-558 ◽  
Author(s):  
BL Evatt ◽  
JL Spivak ◽  
J Levin

Abstract The effects of administration of partially purified human urinary erythropoietin and rabbit thrombopoietin, and of endogenously produced erythropoietin and thrombopoietin on both red cell and platelet production were examined in mice. Partially purified thrombopoietin was prepared from rabbit plasma by sequential fractionation with ammonium sulfate precipitation, and DEAE and Sephadex G-100 chromatography. Preparations of thrombopoietin and partially purified human urinary erythropoietin (NIH No. H-11-TaLSL) were administered subcutaneously to normal mice, and the rate of incorporation of selenomethionine-75 Se into platelets was measured as an index of thrombopoietic activity of the infused material. Erythropoietin and thrombopoietin were assayed for erythropoietic activity by measuring the rate of appearance of 59Fe in the red cells of posthypoxic polycythemic mice. Preparations containing thrombopoietin had barely measurable erythropoietic activity, and 7 units of partially purified erythropoietin had little thrombopoietic activity. When endogenous levels of erythropoietin were increased by hypoxia, platelet production was not enhanced. Similarly, increased levels of thrombopoietin, induced in response to thrombocytopenia produced by platelet antiserum, did not alter red cell production. These data suggest that physiologically increased levels of thrombopoietin do not stimulate erythropoiesis, and that physiologically increased levels of erythropoietn do not stimulate thrombopoiesis. However, currently available, partially purified preparations of erythropoietin and thrombopoietin may be capable of stimulating both platelet and red cell production if used in sufficient quantities.


Blood ◽  
1959 ◽  
Vol 14 (4) ◽  
pp. 386-398 ◽  
Author(s):  
ALLAN J. ERSLEV ◽  
Elva Ruiz

Abstract The action of an anoxic stimulus on red cell production was studied in rabbits bled 20 ml./Kg., kept anemic for 20 hours and then reinfused with the previously removed blood. This 20-hour period of anemic anoxia was followed by a characteristic reticulocyte response, a response which was modified by nitrogen mustard or colchicine administered immediately after the 20-hour period of anemia, but was not influenced by anoxia or hyperoxia in the postanemic period. When mitotic division was arrested by colchicine during the 20-hour period of anemic anoxia, the onset of the reticulocyte response, though delayed by 1 to 2 days, was otherwise of characteristic magnitude. These observations indicate that (1) the anoxic stimulus operates in the bone marrow by accelerating the differentiation of stem cells into pronormoblasts, and that thereafter (2) the maturation and multiplication of differentiated nucleated red cells proceed at fixed rates independent of the anoxic stimulus.


Blood ◽  
1961 ◽  
Vol 18 (1) ◽  
pp. 61-72 ◽  
Author(s):  
MIGUEL LAYRISSE ◽  
ALFREDO PAZ ◽  
NORMA BLUMENFELD ◽  
MARCEL ROCHE ◽  
Iris Dugarte ◽  
...  

Abstract Iron metabolism, balance of red cell production and destruction and iron absorption from hemoglobin were determined in 11 patients with heavy hookworm infection and severe anemia. The plasma iron, total iron binding capacity, bone marrow hemosiderin and plasma Fe59 clearance are in agreement with the idea that the anemia associated with hookworm infection is of the iron deficiency type. The rate of red cell production measured by the E/M ratio, absolute reticulocyte count and plasma iron turnover showed an increase to about twice normal, while the rate of destruction estimated by the T ½ erythrocyte survival showed a destruction about 5 times normal. This unbalance between production and destruction could explain the severity of the anemia. The increase of fecal urobilinogen output to twice normal was interpreted as due to the metabolism of the hemoglobin lost into the intestine rather than to an increase of hemolysis. The estimation of fecal blood loss in the patients whose red cells were tagged with Cr51 and Fe59, showed that the radioactivity counted with Fe59 was only about 63 per cent of the radioactivity counted with Cr51. This difference was interpreted as due to iron absorption from the hemoglobin lost into the intestine. The mean daily fecal excretion of iron reaches 4.7 mg. Since the iron metabolism in these patients is in equilibrium, we have concluded that the iron loss is replaced by the iron from food; this is in addition to the 3 mg. hemoglobin iron which is reabsorbed from the blood lost into the gut.


Blood ◽  
1961 ◽  
Vol 18 (6) ◽  
pp. 727-736 ◽  
Author(s):  
GERALD A. MENDEL

Abstract (1) Evidence is presented that the augmentation of iron absorption from the gastro-intestinal tract produced by hypoxia can occur independently of acceleration of erythropoiesis. (2) It is demonstrated that the hormone erythropoietin is capable of enhancing iron absorption; and that this property of erythropoietin is indirect, being dependent on acceleration of erythropoiesis. (3) An experimental model for the study of those factors that affect iron absorption and are independent of increased red cell production is presented.


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