Brain amino acids decrease in chronic hyponatremia and rapid correction causes brain dehydration: possible clinical significance.

Abstract

In animals, rapid correction of chronic hyponatremia produces brain lesions similar to those seen in central pontine myelinolysis. This is the first study of the effects of rapid correction (9 h) of chronic hyponatremia (3 d) on brain electrolyte, water, and amino acid contents in young mice. Despite profound hyponatremia, decreases in brain electrolytes and amino acids permitted an apparent osmotic balance between blood and brain with a normal brain water content. Rapid elevation of the depressed plasma sodium concentration to normonatremic levels caused dehydration of the brain. Although brain Na+ and K+ levels were returned to normal, the relatively brief interval of treatment was insufficient to allow complete recovery of brain amino acid levels. Findings support an osmotic disequilibrium--plasma osmolality higher than brain--in the pathogenesis of the brain lesions following rapid correction of chronic hyponatremia and suggest caution in the rate of elevation of the depressed plasma Na+ levels.