Showing papers by "Rosalyn S. Yalow published in 1955"

Distribution and metabolism of i131 labeled human serum albumin in congestive heart failure with and without proteinuria

Abstract: The role of serum albumin in the causation of cardiac edema has been disputed. Starling (1) postulated that circulatory stasis resulting from cardiac insufficiency is responsible for anoxia and increased permeability of the capillary membrane, the consequence of which is the passage of albumin and water into the extravascular spaces. Although Smirk (2) observed evidence of increased capillary permeability to water and crystalloids in congestive heart failure, Stead and Warren (3) demonstrated, by direct analysis, that the protein concentration of cardiac edema fluid was not elevated above that of the edema fluid produced by tourniquet stasis in normal subjects. Other studies have directed attention to the low serum albumin concentrations occasionally encountered in heart failure (4-7), and have suggested or implied (4, 8) a causal relationship to the pathogenesis of cardiac edema. Abnormalities in liver function tests and morphologic evidence of liver injury in severe congestive failure (9-14) have appeared to strengthen the possibility that hepatic synthesis of albumin may be impaired in this condition. Alternatively, low serum albumin concentrations have been attributed to inadequate dietary protein intake or poor absorption from a congested gastrointestinal tract (15, 16). Since the plasma concentration of albumin is not an adequate measure of the total quantity of circulating and extravascular albumin stores, it was of interest to measure the amount of total exchangeable albumin in subjects with heart failure employing I'8l labeled albumin as a tracer. The rate of metabolism of I18l labeled albumin was also studied with the aim of evaluating the ability of the subject in heart failure to synthesize albumin. Although there may yet remain some reservations regarding the validity of this tracer in the

The iodide trapping and binding functions of the thyroid

Abstract: McGinty and Sharp (1) demonstrated that the thyroid glands of rats treated with propylthiouracil retained the ability to concentrate iodide ion but failed to bind the iodine in an organic form. VanderLaan and VanderLaan (2) and Stanley and Astwood (3) showed also that thyroidal io-dide, \"trapped\" under the influence of the anti-thyroid drugs, could be rapidly discharged from the gland by the administration of thiocyanate ion. Iodine accumulation by the thyroid has therefore been considered a two-step function; the first is concerned with the concentration (trapping) of iodide at a level higher than that in the circulating plasma, while the second, in itself a complicated process composed of several chemical stages, is represented by organic binding of the trapped iodide. Several authors have inquired into the kinetics of thyroidal iodide trapping and binding (4-6). On the assumption that equilibration of plasma and thyroidal inorganic iodide131 (iodide trapping) is instantaneous following intravenous administration of 1131, Ingbar (4, 5) calculated that thy-roidal binding of trapped iodide proceeded at average rates of 1% per cent per minute in eu-thyroid subjects and 6% per cent per minute in patients with Graves' disease. Wollman (6) assumed that the plasma iodide131 concentration remained constant or decreased at a single exponential rate and considered the sequelae of several theoretical alternatives for the relative rates of trapping and binding. In the present study an analysis is presented which permits evaluation of the rates of trapping and binding from observed data without assumptions regarding either process or restrictions in the behaviour of the plasma io-dide131 concentration. The results of the experimental investigations indicate an extremely rapid binding of trapped iodide in the untreated gland and lead to the conclusion that trapping rather than binding is the rate-limiting step of thyroidal iodine accumulation. Subjects received intravenous injections of 15 to 200 pc carrier-free NaTls1 in normal saline solution. Assay of thyroidal radioactivity was performed with a bismuth-walled Geiger counter and a scaling circuit connected to a Streeter-Amet register which automatically printed the cumulative counts at minute intervals, as previously described (7). The sensitivity of this arrangement was 110 counts per minute per ,uc I'3 above a background of 60 counts per minute. Five ml. samples of packed erythro-cytes, plasma and urine were counted in a well-type scin-tillation counter with a sensitivity of 1.00 X 106 counts per minute per,c I'l above a background of 200 counts per minute. PBI3s and …