Trachtman H, Barbour R, Sturman J A, Finberg L
Department of Pediatrics, State University of New York, Health Science Center, Brooklyn.
Pediatr Res. 1988 Jan;23(1):35-9. doi: 10.1203/00006450-198801000-00008.
We studied the effect of 8-wk dietary taurine depletion on the vulnerability to hypernatremic dehydration in postweanling kittens. While experimental taurine depletion was not associated with increased susceptibility to acute hypernatremia (1.5 M NaCl/NaHCO3, 35 ml/kg body weight, single injection), there was an increase in mortality (five of seven versus one of seven, p = 0.05) and seizure activity (three of seven versus none of seven, p = 0.08) in taurine-depleted compared to taurine-replete kittens rendered chronically hypernatremic over 96 h. Furthermore, there was a significant decrease in brain cell water (517.4 +/- 21.7 versus 671.6 +/- 32.3 ml/100 g fat-free dry weight, p less than 0.05), derived almost exclusively from the intracellular compartment (352.5 +/- 12.3 versus 483.8 +/- 34.6 ml/100 g fat-free dry weight, p less than 0.05) that correlated with the reduction in the cerebral taurine content in the taurine-depleted versus control kittens during chronic hypernatremic dehydration. These results suggest that taurine is an important cerebral osmoprotective molecule. This aminoacid constitutes nearly 50% of the adaptable intracellular osmolal pool whose concentration varies in the course of osmoregulating in response to perturbations in the extracellular fluid tonicity.
