title: 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.
authors.affiliation: Research Unit for the Study of Hydromineral Metabolism, Faculty of Medicine, Department of General Internal Medicine, Erasme Hospital, Université Libre de Bruxelles, Bruxelles, Belgium. fgankamk@ulb.ac.be
authors.forename: Fabrice
authors.initials: F
authors.lastname: Gankam Kengne
authors.forename: Alain
authors.initials: A
authors.lastname: Soupart
authors.forename: Roland
authors.initials: R
authors.lastname: Pochet
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Brion
authors.forename: Guy
authors.initials: G
authors.lastname: Decaux
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects; D003907:Dexamethasone / Q000627:therapeutic use; D007010:Hyponatremia / Q000150:complications / Q000401:mortality / Q000628:therapy*; D007074:Immunoglobulin G / Q000032:analysis; D008297:Male; D017590:Myelinolysis, Central Pontine / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D009997:Osmotic Pressure; D010539:Permeability; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000097:blood
chemical_list: D007074:Immunoglobulin G; D003907:Dexamethasone; D012964:Sodium