Increased permeability of a glial blood-brain barrier during acute hyperosmotic stress.
Brain volume is regulated during acute hypernatremia in the little skate, Raja erinacea, based on the gain of osmolytes, including sodium, chloride, and potassium [Cserr et al., Am. J. Physiol. 245 (Regulatory Integrative Comp. Physiol. 14): R853-R859, 1983]. In this study we show that this volume regulatory response is complete in 35 min and examine the mechanism of sodium influx across the blood-brain barrier over this period. Skates have a glial blood-brain barrier. Blood-to-brain transfer constants (K1) for 22Na and [14C]mannitol were measured using the integral technique of [Ohno et al.Am. J. Physiol. 235 (Heart Circ. Physiol. 4): H299-H307, 1978]. In skates injected intramuscularly with isotonic saline (controls) or with hypertonic NaCl or fructose, K1 for sodium increased linearly with osmolality. This increase was the same for hypernatremia and fructose-induced hypertonicity, and it was not affected by the "loop" diuretic bumetanide. K1 for mannitol also increased with osmolality. These results suggest that hypertonicity increases barrier permeability by a nonselective mechanism. The contribution of influx across the blood-brain barrier to tissue sodium gain during acute hypernatremia is assessed using a diffusional model of plasma-brain exchange.[1]References
- Increased permeability of a glial blood-brain barrier during acute hyperosmotic stress. Mackie, K., DePasquale, M., Cserr, H.F. Am. J. Physiol. (1986) [Pubmed]
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