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Cerebral cell volume regulation during hypernatremia in developing rats.

Abstract

Cell volume regulation is a vital biological function in all species. Maintenance of cerebral cell size in the face of osmotic stress is especially important because the brain is contained in the non-complaint skull. The developmental aspects of this adaptive process are not known. Therefore, we evaluated cerebral cell volume regulation during hypernatremia in pre-weaning and adult rats. Hypernatremia was induced by injections of 1 M NaCl for 48 h. Brain water, electrolyte, and organic osmolyte contents were measured in hypernatremia and sham injected littermate control rats at the following ages: 12, 18 and 20 days and adults. In normonatremic rats, there was a steady decline in brain water content during development that was paralleled by a gradual fall in the cerebral levels of Na+, K+, and all organic osmolytes. The change in brain water content correlated most closely with the decrease in cerebral taurine content. In the face of equivalent elevations in serum Na+ concentration, there was comparable brain cell shrinkage and similar increases in total cerebral electrolyte and organic osmolyte content in rats at all 4 ages studied. Taurine was the predominant organic osmolyte prior to weaning, constituting 16-49% of the increment in nonperturbing solute content in hypernatremic animals between 12-20 days of age; in contrast, taurine contributed only 10% to the cerebral organic osmolyte pool in adult rats. We conclude that the capacity of brain cells to accumulate inorganic electrolytes and organic osmolytes during adaptation to hypernatremia is adequately expressed in developing rats, aged 12 days or older. Moreover, we speculate that the immature animal behaves as if it has an elevated 'set point' to protect the higher brain water content that is present earlier in development.

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BibTeXRIS

H Trachtman, P H Yancey, S R Gullans. 1995-09-25. Cerebral cell volume regulation during hypernatremia in developing rats.. https://doi.org/10.1016/0006-8993(95)00650-f

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