The frequently used intraperitoneal hyponatraemia model induces hypovolaemic hyponatraemia with possible model-dependent brain sodium loss

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Overgaard-Steensen, ChristianAarhus Univ Hosp NBG, Dept Anaesthesiol, Aarhus, Denmark.;Aarhus Univ, Aarhus Univ Hosp, Inst Clin Med, Skejby, Denmark. (författare)

The frequently used intraperitoneal hyponatraemia model induces hypovolaemic hyponatraemia with possible model-dependent brain sodium loss

Artikel/kapitelEngelska2016

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2016
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LIBRIS-ID:oai:DiVA.org:uu-303388
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-303388URI
https://doi.org/10.1113/EP085751DOI

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Språk:engelska
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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 (I.P. 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 I.P. model in a large animal (the pig) and studied water and electrolyte responses in brain, muscle, plasma and urine. We hypothesized that hyponatraemia was induced by simple water dilution, with no change in organ sodium content. Moderate hypotonic hyponatraemia was induced by a single I.V. dose of desmopressin and intraperitoneal instillation of 2.5% glucose. All animals were anaesthetized and intensively monitored. In vivo brain and muscle water was determined by magnetic resonance imaging and related to the plasma sodium concentration. Muscle water content increased less than expected as a result of pure dilution, and muscle sodium content decreased significantly (by 28%). Sodium was redistributed to the peritoneal fluid, resulting in a significantly reduced plasma volume. This shows that the I.P. model induces hypovolaemic hyponatraemia and not dilutional/SIADH hyponatraemia. Brain oedema evolved, but brain sodium content decreased significantly (by 21%). To conclude, the I.P. model induces hypovolaemic hyponatraemia attributable to sodium redistribution and not water dilution. The large reduction in brain sodium is probably attributable 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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Stodkilde-Jorgensen, HansAarhus Univ Hosp, MR Res Ctr, Skejby, Denmark. (författare)
Larsson, AndersUppsala universitet,Hedenstiernalaboratoriet,Anestesiologi och intensivvård(Swepub:uu)andla606 (författare)
Tonnesen, ElseAarhus Univ Hosp NBG, Dept Anaesthesiol, Aarhus, Denmark.;Aarhus Univ, Aarhus Univ Hosp, Inst Clin Med, Skejby, Denmark. (författare)
Frokiaer, JorgenAarhus Univ, Aarhus Univ Hosp, Inst Clin Med, Skejby, Denmark.;Aarhus Univ, Water & Salt Res Ctr, Aarhus, Denmark. (författare)
Ring, TroelsAalborg Univ Hosp, Dept Nephrol, Aalborg, Denmark. (författare)
Aarhus Univ Hosp NBG, Dept Anaesthesiol, Aarhus, Denmark.;Aarhus Univ, Aarhus Univ Hosp, Inst Clin Med, Skejby, Denmark.Aarhus Univ Hosp, MR Res Ctr, Skejby, Denmark. (creator_code:org_t)

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Ingår i:Experimental Physiology101:7, s. 932-9450958-06701469-445X

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Av författaren/redakt...: Overgaard-Steens ...; Stodkilde-Jorgen ...; Larsson, Anders; Tonnesen, Else; Frokiaer, Jorgen; Ring, Troels

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