Perturbations in glucose homeostasis expose premature and full term neonates to hyperglycemic hyperosmolality which may alter brain volume (water) regulation. We have previously demonstrated that during an acute osmotic stress with the non-metabolizable sugar mannitol, in contrast to adult sheep, fetuses and lambs do not exhibit volume regulation in most brain regions(Pediatr Res 37:239A, 1995). We extended this work to study regional brain water responses to glucose-induced acute hyperosmolality in chronically instrumented (1) fetuses at 60% of gestation (87 days, n = 20), (2) cesarean section-delivered, surfactant-treated, ventilated premature lambs at 90% gestation (137 days, n = 16), (3) newborn lambs (4 day old, n = 12) and (4) adult sheep (2 year, n = 16). After exposure to graded increases in systemic osmolality, regional brain water was quantified by standard techniques. In the absence of volume regulation, brain solute remains constant as osmolality changes (Fig., ---). As opposed to our findings with mannitol, brain volume regulation during glucose-induced hyperosmolality was present (Fig., p<0.05) in all regions in fetuses at 60% of gestation, in premature lambs, and in all regions except for the caudate nucleus in newborn lambs and the cerebellum and midbrain in adult sheep. We speculate that active glucose transport and metabolism increases the solute concentration in brain tissue thus limiting water loss in response to a systemic osmotic load. (NIH P50 HD 11343)

figure 1

Figure 1