Abstract
Hyponatraemia is common clinically, and if it develops rapidly, brain oedema evolves, and severe morbidity and even death may occur. Experimentally, acute hyponatraemia is most frequently studied in small animal models in which the hyponatraemia is produced by intraperitoneal instillation of hypotonic fluids (IP-model). This hyponatraemia model is described as "dilutional" or "syndrome of inappropriate ADH (SIADH)", but seminal studies contradict this interpretation. To confront this issue, we developed an IP-model in a large animal (pig) and studied water and electrolyte responses in brain, muscle, plasma and urine. We hypothesised that hyponatraemia was induced by simple water dilution, with no change in organ sodium content. Moderate hypotonic hyponatraemia was induced by a single IV dose of desmopressin and intraperitoneal instillation of 2.5% glucose. All animals were anaesthetised and intensively monitored. In vivo brain and muscle water was determined by magnetic resonance imaging and related to plasma sodium concentration. Muscle water content increased less than expected due to pure dilution, and muscle sodium content decreased significantly (28%). Sodium was redistributed to the peritoneal fluid, resulting in a significantly reduced plasma volume. This shows that the IP-model induces hypovolaemic hyponatraemia and not dilutional/SIADH hyponatraemia. Brain oedema evolved, but brain sodium content decreased significantly (21%). To conclude, the IP-model induces hypovolaemic hyponatraemia due to sodium redistribution and not water dilution. The large reduction in brain sodium is probably due to the specific mechanism that causes the hyponatraemia. This is not accounted for in the current understanding of the brain response to acute hyponatraemia.
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