BLOOD-BRAIN-BARRIER TAURINE TRANSPORT DURING OSMOTIC-STRESS AND IN FOCAL CEREBRAL-ISCHEMIA

Little is known about blood to brain taurine transport despite substan tial evidence suggesting a role of taurine in brain volume regulation during osmotic stress or conditions inducing cell swelling, such as is chemia. We have made measurements of the taurine influx rate constant (K-1) with [H-3]taurine in three conditions: raised plasma taurine con centrations induced by infusion with 50 mM taurine (10 mu l/100 g/min) ; osmotic stress induced by i.p. injections of 1.5 M NaCl (2 ml/100 g) or distilled water (10 ml/100 g); and 4 h of middle cerebral artery o cclusion (MCAo). In rats with MCAo, additional determinations were mad e of tissue water and taurine contents, and blood-brain barrier passiv e permeability with [H-3]alpha-aminoisobutyric acid. Taurine infusion increased plasma taurine from 110 +/- 63 mu M (SD) to 407 +/- 63 (p < 0.001) and decreased taurine K-1 at the blood-brain barrier by 70% (p < 0.001), signifying saturable uptake that maintained unidirectional i nflux constant. Similarly, although hypo- and hyperosmolality increase d and decreased plasma taurine concentration, respectively, a reciproc al relationship between K-1 and plasma taurine in these experiments en sured that unidirectional fluxes of taurine into brain were unchanged by osmotic stress. During MCAo, the taurine K-1 was reduced 80% in the ipsilateral ischemic tissue compared with the contralateral nonischem ic tissue (p < 0.001). This decline may be due to a release of taurine into the brain circulation, because there was a concomitant loss of t issue taurine of 7.4 +/- 2.4 mmol/g dry weight (p < 0.05). Alternately , if taurine uptake is sodium dependent, the decline might reflect a d isruption of the endothelial sodium gradient.