Treatment of hyponatraemia by urea decreases risks of brain complications in rats. Brain osmolyte contents analysis

Background. Brain damage (myelinolysis) develops in hyponatraemia after a large increase in serum sodium regardless of the currently available methods of correction. However, a preliminary study suggests that treatment of hyponatraemia with urea limits the risks of brain lesions in rats. Benefits of...

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Bibliographic Details
Published in:Nephrology, dialysis, transplantation dialysis, transplantation, 2007-07, Vol.22 (7), p.1856-1863
Main Authors: Soupart, Alain, Schroëder, Barbara, Decaux, Guy
Format: Article
Language:English
Subjects:
Amyloidosis
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Betaine - metabolism
Biological and medical sciences
Body Water - metabolism
brain
Brain - metabolism
Brain Diseases - etiology
Brain Diseases - prevention & control
Demyelinating Diseases - etiology
Demyelinating Diseases - prevention & control
Electrolytes - metabolism
Emergency and intensive care: renal failure. Dialysis management
Endocrinopathies
hyponatraemia
Hyponatremia - blood
Hyponatremia - complications
Hyponatremia - drug therapy
Hyponatremia - mortality
Hypothalamus. Hypophysis. Epiphysis (diseases)
Intensive care medicine
Male
Medical sciences
Metabolic diseases
Non tumoral diseases. Target tissue resistance. Benign neoplasms
osmotic demyelinating syndrome
Other metabolic disorders
Rats
Rats, Wistar
Sodium - blood
urea
Urea - blood
Urea - therapeutic use
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Summary:Background. Brain damage (myelinolysis) develops in hyponatraemia after a large increase in serum sodium regardless of the currently available methods of correction. However, a preliminary study suggests that treatment of hyponatraemia with urea limits the risks of brain lesions in rats. Benefits of sustained high blood levels of urea and mechanisms of protection remain hypothetical. Methods. In the first part of the study, hyponatraemic rats received repeated (i.p.) doses of urea (2 g/kg b.w./6 h) leading to sustained blood levels (urea ± 230 mg/dl). Neurologic outcome was compared to correction of hyponatraemia by water diuresis. In the second part of the study, we analysed the adaptative response of the brain to correction of hyponatraemia with either urea or water diuresis, by measurement of cerebral osmolyte contents. Results. Despite a large correction of the serum sodium (mean Δ SNa = 32 mEq/l/24 h), mortality rate (13%) and neurological symptoms were low in the urea-treated group contrary to control groups treated by water diuresis (mortality: 87%). This shows with stronger evidence the protective effect of urea against brain myelinolysis. In the second part, analysis of brain composition shows that, in the urea groups, 24 h after correction, intracerebral hyperionization (NaCl) was avoided and brain water contents remained normal. No significant changes of the major brain organic osmolyte composition were observed after urea administration except reaccumulation of betaine. No difference in brain composition was noted regarding concomitant plasma urea levels (> or
ISSN:0931-0509
1460-2385
DOI:10.1093/ndt/gfm138