Effect of acute and chronic hyponatremia on brain buffering in rats.

The present studies evaluated whether previously observed impairments in brain buffering during acute hyponatremia were maintained during chronic hyponatremia as well and whether the impairment was due in part to changes in brain water, brain perfusion, or activation of arginine vasopressin (AVP) V1 receptors. Acute (1 and 2 day) and chronic (7 and 14 day) hyponatremia was induced in male Sprague-Dawley rats by constant desmopressin administration in combination with a liquid diet. Brain pH was determined by 31P nuclear magnetic resonance (NMR) in rats anesthetized with N2O and paralyzed with pancuronium. Brain buffering was evaluated by the response to CO2 loading, and brain perfusion was evaluated by 19F-NMR using trifluoromethane washout. Compared with normonatremic controls fed the same diet, brain pH in both acute and chronic hyponatremics was 0.12 pH units lower after 55 min ventilation with 20% CO2 despite identical decreases of approximately 0.35 units in all groups during the first 15 min. Moreover, in the recovery period brain pH overshot basal levels only in normonatremic controls. Brain water content in chronic hyponatremic rats was equal to controls, and brain perfusion was identical in the five groups during CO2 exposure. These results are analogous to those reported during acute hyponatremia induced with AVP and show that the impairment of active brain buffering is maintained during chronic hyponatremia and is unrelated to brain water content, perfusion, tissue catabolism, or AVP V1 receptor activation.