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Decreased renal excretion of sodium is a wellknown feature of the immediate postoperative state (1-3). The mechanisms responsible have, however, not been clearly defined. While increased adrenal cortical secretion such as is generally associated with major surgical procedures (4-9) has been causally implicated by many investigators (1, 3, 10-13), there is considerable evidence that the changes in sodium excretion are independent of variations in the supply of adrenal cortical hormones (14-18). The extracellular fluid volume, or more precisely that portion of it which is physiologically "effective," has been shown to be a major determinant of renal sodium excretion in normal individuals (19-21). Therefore variation in this volume warrants consideration as a possible etiological factor in the decreased postoperative excretion of sodium. The observations that fluid sequestration occurs in and about the traumatized tissues both in animals and in man indeed suggests that a dislocation of the body fluids may occur in the surgical patient and result in a contraction of the effective extracellular fluid volume. The present study was designed to investigate the effect of isotonic expansion of the extracellular fluid volume on the postoperative response to the administration of sodium chloride. The data indicate that the usually observed impairment in natriuretic response is corrected by isotonic extracellular fluid volume expansion. In addition, studies in a patient with Addison's disease suggest that decreased natriuresis postoperatively occurs independently of enhanced adrenal cortical hormone secretion.

Mechanism of Postoperative Limitation in Sodium Excretion: The Role of Extracellular Fluid Volume and of Adrenal Cortical Activity1