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