SEVERE BRAIN EDEMA ASSOCIATED WITH CUMULATIVE EFFECTS OF HYPONATREMICENCEPHALOPATHY AND ISCHEMIC HYPOXIA

Hyponatremia in cats produced brain edema, detectable by both magnetic resonance imaging (MRI) and increased brain water, with a compensator y decrease of brain sodium. Sodium transport was measured in synaptoso mes from hyponatremic cat cerebral cortex. The sodium efflux via Na+-K +-ATPase was significantly higher (144%) than control, while sodium in flux via the Na+/H+ antiporter was significantly decreased (74%). Both responses tend to decrease brain intracellular sodium and thus, brain cell osmolality. Ischemia following unilateral middle cerebral artery occlusion also resulted in brain edema. However, the efflux of sodium via both Na+-K+-ATPase and sodium channels actually decreased, both m aladaptive responses. Furthermore, when ischemia was superimposed upon hyponatremia, all of the cerebral adaptive changes which had been ind uced by hyponatremia alone were rendered ineffective. This resulted in further elevations of brain water and sodium. Hyponatremia superimpos ed upon ischemia thus worsens the brain edema associated with ischemia alone. Thus, ischemia impairs the ability of the brain to adapt to hy ponatremia, probably by eliminating the compensatory mechanisms of bra in sodium transport initiated by hyponatremia.