Chronic hypoxemia was induced in one partner of a pair of parabiotic rats by exposure to defined gas mixtures with low oxygen content. The other partner of the pair was kept in normal atmosphere throughout the experiment and showed normal values of the oxygen saturation of the blood. The erythropoiesis, estimated by the percentage of nucleated red cells in the bone marrow, showed a statistically significant stimulation in both animals. It is, therefore, concluded that under these experimental conditions, the stimulus is not the partial pressure of oxygen in the bone marrow directly but a humoral factor elicited by the hypoxemia in the one partner and transferred to the other one.

An elevated serum iron is commonly found in patients with infectious hepatitis (1-4) and evidence has been presented (5, 6) that acute hepatocellular necrosis, regardless of its etiology, is invariably accompanied by a rise in serum iron. A close time relationship between elevation of the serum iron and actual disintegration of liver cells has been found (6), and the hyperferremia has been attributed to a release of storage iron from the dying liver cells. As the iron is largely stored in the liver as ferritin, it was of interest to investigate whether ferritin is released into the peripheral blood of patients with acute hepatocellular disease, while it could not be demonstrated in the blood of normal individuals (7).Mazur, Shorr, and Baez (8-10) have reported the presence of VDM, which is said to be identical with ferritin, in the peripheral blood in several conditions including hepatic cirrhosis, congestive heart failure and shock. The concentrations of this vasoactive material were so minute that their detection required the use of the mesoappendix bioassay. We were, in this study, concerned with a possible relationship between serum iron rise and the release of ferritin iron from the necrotic liver cells. METHODSCrystalline ferritin-apoferritin was prepared from human liver tissue (autopsy material) according to the method of Granick (7). The crude ferritin was recrystallized five times with CdSO4, reprecipitated at 50 per cent saturation with (NH4),SO4, and dialyzed against tap water for 24 hours. At that time the preparation was usually free of NH4 ions.The antiserum was prepared according to the procedure of Mazur and Shorr (8). Rabbits were injected intravenously with aluminum precipitated human ferritin over a period of four weeks. Each animal received a total of 4.4 mg. of antigen nitrogen, and thereafter booster injections of 0.15 mg. of antigen nitrogen. The antisera were chilled, sharply centrifuged and pooled. The antiferritin titer of the antiserum was determined by adding known amounts of ferritin dissolved in human serum to one cc. of the 1: 10 diluted antiserum. The mixture was incubated for one hour at 370 C. and stored for three days at 40 C. The tubes were then centrifuged, the precipitate washed with chilled saline, and the iron and nitrogen in the precipitate were measured. The supernatant was tested for excess of antigen or antibody.The iron content of ferritin was measured by Scott's method (11). Other iron methods employed were the methods of Wong (12), of Barkan and Walker (13) and a modification of the latter as described below.The ferritin determination in the blood of patients was carried out in the following manner: The blood was collected in iron free tubes and the serum was sharply centrifuged to remove all red cells. Four cc. of this serum was added to 0.3 of antiserum, to 0.3 of 1: 3 diluted antiserum, and to 0.3 cc. of normal rabbit serum, respectively.After one hour of incubation at 370 C. and three days' storage at 4°C., the tubes were centrifuged. When ferritin was present...

No abstract

The oxygen consumption of the beating dog heart, performing no external work, was measured in modified Langendorf preparations. Increasing heart rates, induced by rewarming of the cooled sinus node, were associated with linear increments in oxygen consumption. By extrapolation of these measurements, an average cardiac maintenance metabolism at zero rate of 1.98 cc O2/min. and 100 gm heart weight was found. Above this resting metabolism the energy cost of contraction at zero external work amounted to from .83 to 1.18 cc O2/100 beats and 100 gm heart. Measurements of the cardiac oxygen consumption during constant external work per unit of time and while the same heart was performing no external work directly demonstrated the decreased energy cost of external work at slower heart rates.

A single administration of Myleran eradicated colony-forming stem cells from marrow or spleen of mice for a period of two weeks or longer. Erythropoiesis was restored during that time, and the exclusion of cell influx from the colony-forming progenitors into the intermediary erythroid stem cell compartment permitted a study of the effects of erythropoietin on the kinetics of the latter. The results indicate that erythropoietin, in addition to its role in transforming immediate precursors into proerythroblasts, stimulated the proliferation of erythroid stem cells. The significance of this in regard to stem cell kinetics and rate regulation of erythropoiesis is discussed.