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Re-induction of hyponatremia after rapid overcorrection of hyponatremia reduces mortality in rats.

Abstract
Osmotic demyelination syndrome is a devastating neurologic disorder often seen after the rapid correction of chronic hyponatremia. The permeability of the blood-brain barrier is increased in experimental osmotic demyelination, and some have suggested that corticosteroids protect against this disorder by keeping the permeability of the blood-brain barrier low. We previously reported that re-lowering of the serum sodium after rapid correction of chronic hyponatremia was beneficial if performed early in the course (12 to 24 h). Here we compared mortality, blood-brain barrier permeability, and microglial activation in rats after the rapid correction of chronic hyponatremia. We studied three groups of rats after correction of chronic hyponatremia: and treated them with sodium chloride, with or without dexamethasone; or with sodium chloride followed by re-induction of hyponatremia. We found that treatment with dexamethasone or re-induction of hyponatremia effectively prevented the opening of the blood-brain barrier, reduced neurological manifestations, and decreased microglial activation; however, only re-induction of hyponatremia resulted in a significant decrease in mortality 5 days after the correction of chronic hyponatremia. Restoring the permeability of the blood-brain barrier to normal levels did not decrease mortality. Our results suggest that after inadvertent rapid correction of hyponatremia, treatment options should favor re-lowering serum sodium. The increased permeability of blood-brain barrier seen in osmotic demyelination syndrome may not be a primary pathophysiologic insult of this syndrome.
AuthorsFabrice Gankam Kengne, Alain Soupart, Roland Pochet, Jean-Pierre Brion, Guy Decaux
JournalKidney international (Kidney Int) Vol. 76 Issue 6 Pg. 614-21 (Sep 2009) ISSN: 1523-1755 [Electronic] United States
PMID19606078 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Immunoglobulin G
  • Dexamethasone
  • Sodium
Topics
  • Animals
  • Blood-Brain Barrier (drug effects)
  • Dexamethasone (therapeutic use)
  • Hyponatremia (complications, mortality, therapy)
  • Immunoglobulin G (analysis)
  • Male
  • Myelinolysis, Central Pontine (etiology, physiopathology, therapy)
  • Osmotic Pressure
  • Permeability
  • Rats
  • Rats, Wistar
  • Sodium (blood)

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