Taurine and osmoregulation. II. Administration of taurine analogues affords cerebral osmoprotection during chronic hypernatremic dehydration
Trachtman, H.; Del Pizzo, R.; Sturman, J.A.; Huxtable, R.J.; Finberg, L.
American Journal of Diseases of Children 142(11): 1194-1198
1988
ISSN/ISBN: 0002-922X PMID: 3177325 Document Number: 315371
We have previously shown that in the cat, taurine is an osmoprotective molecule that lessens mortality, neurological morbidity, and brain-cell dehydration during chronic hypernatremic dehydration. We examined the ability of two taurine analogues to afford cerebral osmoprotection in rats. Pretreatment with guanidinoethane sulfonate, a competitive antagonist for .beta.-amino acid transport, as a 1% drinking solution for ten days led to a significant reduction in brain-cell dehydration. Thus total brain-cell water was higher in experimental vs control animals (544.3 .+-. 36.8 vs 478.2 .+-. 12.7 mL/100 g of fat-free dry solids [FFDS]) and the difference was almost exclusively derived from the intracellular water compartment (452.7 .+-. 27.3 vs 371.4 .+-. 7.7 mL/100 g of FFDS). Pretreatment with taltrimide, a lipophilic taurine derivative (intraperitoneal injection of 200 mg/kg for four days), led to similar results. Total brain-tissue water was significantly higher in experimental vs control rats (507.6 .+-. 18.8 vs 363.2 .+-. 9.5 mL/100 g of FFDS), with the difference primarily derived from the intracellular water space (372.8 .+-. 18.1 vs 221.3 .+-. 13.1 mL/100 g of FFDS). These results suggest that the cerebral response to chronic hypertonic stress includes accelerated transmembrane flux of osmoprotective solutes in addition to mobilization form sequestered intracellular storage sites in an attempt to increase the cytosolic pool of osmotically active molecules.