Changes in cerebral blood flow and distribution associated with acute increases in plasma sodium and osmolality of chronic hyponatremic rats

The cause of the osmotic demyelination syndrome that follows too rapid corr ection of chronic hyponatremia (CHN) is unknown. Recently, we reported in C HN rats an association between blood-brain barrier (BBB) disruption occurri ng as early as 3 h into correction and subsequent demyelination. Given the changes in brain water and blood volume which occur during correction of CH N, we hypothesized that the same correction protocol that causes demyelinat ion might alter cerebral blood how (CBF) during correction, thereby possibl y contributing to BBB disruption and demyelination. Ten CHN rats were given hypertonic sodium intraperitoneally and its effect on CBF was continuously monitored for 3 h by magnetic resonance how imaging. Over the subsequent 3 h, plasma sodium rose from 110.8 to 127.6 mEq/liter (P < 0.001) but neithe r mean arterial blood pressure nor arterial CO2 tension changed significant ly. By 30 min, CBF increased by 50% in cortical and subcortical areas (P < 0.001) and remained elevated for the next 60 min. After 2 h, cortical flow was no longer elevated significantly and by 3 h it had returned to control values. Subcortical flow, however, significantly exceeded control values th roughout the 3 h so that after 2 h the ratio of cortical to subcortical blo od flow had fallen from 1.17 to 0.91 (P < 0.05). Although the mechanism by which increased plasma sodium and osmolality alters CBF is uncertain, the r esults suggest that changes in CBF may be part of a cascade of cerebrovascu lar disturbances including endothelial or parenchymal damage, mechanical ev ents, metabolic disturbances, or cytokine release which eventually lead to BBB disruption and subsequent demyelination. (C) 2000 Academic Press.