The redistribution of fluid and electrolytes was investigated in a hyperdynamic sepsis animal model using cecal ligation and puncture (CLP) in Wistar rats. Hyponatremia was not observed. There was a significant shift of sodium, chloride, and water from the extracellular into the intracellular space as early as 12 hours following CLP. These data suggest that the mechanism by which hyponatremia occurs in clinical sepsis is not caused by shift of fluid from the intracellular to the extracellular space as proposed by the sick cell theory. This is more likely to result from fluid retention and dilution of the extracellular space possibly on the basis of antidiuretic hormone secretion.