Journal
KIDNEY INTERNATIONAL
Volume 69, Issue 8, Pages 1319-1325Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.ki.5000187
Keywords
hypoxia; hyponatremia; cerebral perfusion; cerebral edema; brain histopathology; hypoxic brain damage
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Funding
- NIA NIH HHS [R01 AG 08575-01A2] Funding Source: Medline
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Hypoxia appears to be a prominent component of brain damage among patients with hyponatremic encephalopathy. Effects of hypoxia on brain in the presence of hyponatremia are not known. In order to evaluate the contributions of hypoxia to brain damage, three separate experiments were conducted in three groups of rodents. Experiment I evaluated the effects of hypoxia and acute (<4 h) hyponatremia ( plasma Na <120 mmol/l) on brain adaptation in rabbits. Experiment II evaluated the effects of hypoxia and chronic ( 4 days) hyponatremia on cerebral perfusion in rats. Experiment III evaluated the effects of hypoxia and chronic hyponatremia on brain histology in rats. In experiment I, rabbits with acute hyponatremia demonstrated brain adaptation with significant falls in brain Na content ( by 14.2%, P<0.01) and osmolality ( by 8.3%, P<0.01), and a rise in brain water ( by 10.6%, P<0.05). Rabbits with combined hypoxia and hyponatremia failed to demonstrate brain adaptation. In experiment II, rats with chronic hyponatremia plus hypoxia had a decrease in cerebral perfusion index by more than 50% ( P<0.01). In experiment III, 23% of hypoxic rats had brain lesions, which were in the cerebellum, thalamus, reticular formation, and basal ganglia. Hyponatremia without hypoxia resulted in no brain lesions. Hypoxia in normonatremic animals results in cerebral edema and histopathologic lesions similar to those found in rats whose plasma Na was overcorrected. Hypoxia in hyponatremic animals aggravates cerebral edema, impairs brain adaptation, and decreases cerebral perfusion.
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