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PubMed1955

Stroma protein and stroma lipides vary in different types of anemia.

Normal red blood cells in dogs contain stroma in fairly uniform amounts. This red cell stroma is rich in proteins and lipides. Anemia due to blood loss causes an increase in stroma protein. The highest levels of stroma protein are found in the severe anemias. As the anemia is corrected by red cell regeneration, the stroma protein level falls to normal. Anemia due to blood destruction (phenylhydrazine) presents very high levels of stroma protein-almost double the increase noted in anemia due to blood loss. Hypoproteinemia added to anemia due to blood loss causes no significant change on the stroma protein level. Abscesses due to the subcutaneous injection of turpentine during the anemia cause slight decreases in the stroma protein levels. Chloroform poisoning has no effect on the stroma protein levels. The total lipides of the stroma are rather stable and are little influenced by anemia. In certain experiments with hemolytic anemia and with hypoproteinemia, there is a significant rise in total lipide figures.

Anemia↗
PubMed1955

Red cell stroma and hemoglobin metabolism in anemic dogs; regeneration of red cell proteins labeled with C14 lysine.

Red cell stroma protein and hemoglobin can be labeled by feeding C(14) lysine during periods of active blood regeneration following anemia. Stroma proteins are produced and a maximum concentration of the C(14) label appears 2 to 3 days earlier than with hemoglobin,-which is to say that stroma building precedes hemoglobin construction. The concentration of isotope in stroma protein may exceed its concentration in hemoglobin during regeneration following anemia due to blood loss. Diets favorable for hemoglobin regeneration may force the hemoglobin isotope concentration above that of the stroma protein. In hemolytic anemias great reserves of red cell building material are stored in the body. These stores may modify the curves of isotope concentration in red cells during the recovery periods. When finally formed, the mature red cells show little or no evidence of participation in general body protein metabolism during their life in the circulation.

Anemia↗
PubMed1955

Red cell stroma protein rich in vitamin B12 during active regeneration; anemia studies using radioactive cobalt B12 in dogs.

During active blood regeneration in anemia in dogs an increase occurs in the stroma protein of the red cells. When vitamin B(12) with radioactive cobalt is given at the start of this blood regeneration one finds concentration of labeledB(12)in the stroma protein but not in the hemoglobin. After the acute phase of red cell regeneration is ended the concentration of B(12) in stroma protein falls rapidly to very low levels within 2 weeks. Subsequent episodes of red blood cell regeneration seems not to cause remobilization of radioactive cobalt into red cells from other body stores. It appears that the vitamin B(12) is a factor of importance in the first steps of stroma protein formation in the first few days of the life of the red cell in the dog. This response in dogs and the response in pernicious anemia to vitamin B(12) may have some points in common. Distribution of the B(12)-radioactive cobalt in the organs and tissues at autopsy has been recorded. Some very suggestive localizations were noted and some variation 1 week and 7 weeks after B(12) injections. Radioactive cobalt escapes in the urine during the weeks following B(12) injections.

Anemia↗
PubMed1956

The kinetics of iron metabolism in swine with various experimentally induced anemias.

Ferrokinetic studies were performed on 3 swine given phenylhydrazine, 3 swine deficient in pyridoxine, and 3 swine deficient in pteroylglutamic acid. Body surface radioactivity was measured in 2 pteroylglutamic acid-deficient animals. In the animals given phenylhydrazine, the mean erythrocyte survival time was 5 days. The plasma iron turnover rate was increased about fourfold, and the rate of erythropoiesis was four to five times greater than that in the control pigs. In the pyridoxine-deficient swine, the mean erythrocyte survival time was within the limits of normal. The plasma iron turnover rate was increased fourfold, but the rate of erythropoiesis was approximately one-fourth the normal mean value. These data are interpreted as indicating that the anemia associated with this deficiency is a result of an inability of the bone marrow to produce a normal number of erythrocytes. In the pteroylglutamic acid-deficient swine, the mean erythrocyte survival time was 17 days. The plasma iron turnover rate was 5 times the normal mean value. The rate of erythropoiesis was 1.6 times greater than the mean value in the control pigs. These data are interpreted as indicating that anemia develops in this deficiency as a result of a combination of a shortening of the erythrocyte survival time and a limitation of the capacity of the bone marrow to increase red cell production to the same degree as a normal marrow. The radioactivity in the liver, spleen, and bone marrow of the pteroylglutamic acid-deficient swine, as determined by measurement of the radioactivity over the body surface, declined more slowly than in control pigs.

Anemia↗
PubMed1956

Studies on copper metabolism. XIX. The kinetics of iron metabolism and erythrocyte life-span in copper-deficient swine.

Ferrokinetic studies were performed in three copper-deficient swine and the results have been compared with similar studies in 18 normal pigs. The mean value for the plasma iron turnover rate in the deficient swine was 1.76 mg./kg. day; for the red cell iron incorporation rate, 1.24 mg./kg. day; for the red cell iron turnover rate, 1.18 mg./kg. day; for the red cell life span, 13 days. Corresponding figures in the normal swine were 1.11 mg./kg. day, 1.01 mg./kg. day, 0.59 mg./kg. day and 63 days, respectively. The red cell life span was measured by the use of radioactive chromium in a total of 26 pigs. The mean erythrocyte half-life of normal cells transfused into normal pigs was 17 days. The mean half-life of erythrocytes from copperdeficient swine transfused into copper-deficient swine was 9 days. The mean half-life of red cells from control animals transfused into copper-deficient swine was 16 days while that of erythrocytes from copper-deficient swine transfused into normal pigs, was 13 days. The mean half-life of cells from iron-deficient pigs transfused into iron-deficient pigs was 19 days. It is concluded that copper deficiency anemia results from both a shortened erythrocyte survival time and limited capacity of the bone marrow to produce red cells. It is suggested that copper is an essential component of erythrocytes in swine.

Anemia↗
PubMed1961

Studies on anemia in F1 hybrid mice injected with parental strain lymphoid cells.

The survival of (51)Cr-labeled erythrocytes has been studied in F(1) hybrid mice in which wasting disease was produced by injection of parental lymphoid cells taken either from lymph nodes and thymus or from the spleen. Coincident with the development of the disease syndrome, there occurred a severe anemia accompanied by a sudden loss of circulating labeled erythrocytes, whether host or parental. This finding suggests that the anemia is not due solely to specific immunologic reaction of donor tissue against host erythrocytes.

Anemia↗