Peak rates of diuresis in healthy humans during oral fluid overload

To determine whether rates of intestinal fluid absorption and renal diuresis can match high rates of fluid ingestion in healthy humans exposed to oral fluid overload, thereby preventing the development of hyponatraemia either by reverse sodium movement across the intestine (the Priestley-Haldane effect) or by expansion of the extracellular fluid volume.

Changes in renal function and in plasma chemical measurements in response to an oral fluid overload (0.9-1.8 l/h x 3 h) were investigated in 6 healthy control subjects at rest, and in a subject with a history of exercise-induced symptomatic hyponatraemia, during both prolonged (160-minute) exercise and at rest.

All control subjects gained weight (2.7 +/- 0.2 kg, mean +/- standard error of mean (SEM)) because the rate of oral fluid intake exceeded the peak rate of urine production (778 +/- 39 ml/h). Blood volume rose by 7.1 (+/- 0.5)% and plasma sodium concentrations fell progressively from 144 +/- 2.6 to 136 +/- 1.1 mmol/l (P < 0.05) in the control subjects. Plasma potassium and angiotensin II concentrations were unchanged and creatinine clearance was normal (approximately 125 ml/min). Free water clearance reached a maximum of 11.2 +/- 0.9 ml/min after 2 hours. The increase in body mass could be accounted for by calculated or measured changes in extra- and intracellular fluid volumes. Similar changes were measured in the subject with a previous history of symptomatic hyponatraemia.

The rate of intestinal fluid absorption appeared to match the rate of oral fluid ingestion and there was no evidence of fluid accumulation in the intestine with reverse sodium movement from the extracellular space into intestinal fluid. The results of this study are therefore at variance with the Priestley-Haldane hypothesis and suggest that reverse sodium movement did not contribute to the hyponatraemia induced by oral fluid overload in these subjects. Rather it appears that humans may have a limited capacity to excrete fluid at rates in excess of approximately 900 ml/h in response to higher rates of oral fluid intake. When the rate of intestinal fluid absorption matches the rate of fluid ingestion and exceeds the kidneys' maximum capacity for fluid excretion, the excess fluid accumulates in the extra- and intracellular fluid compartments, inducing the dilutional hyponatraemia of water intoxication. These findings may have relevance to other clinical conditions in which hyponatraemia develops in response to high rates of oral or intravenous fluid provision.