Alterations in the Distribution of Water, Sodium, Potassium, and Chloride in Brain during the Evolution of Ischemic Cerebral Edema

Abstract

Experimental regional cerebral ischemia in the territory of the middle cerebral artery (MCA) in a primate (Macaca mulatta) was produced by selective embolization of the internal carotid artery bifurcation. Determinations of tissue dry weight (percentage) and tissue sodium, potassium, and chloride on samples from the affected and contralateral hemispheres were carried out periodically until 48 hours after the onset of focal cerebral ischemia. Samples from the cortex supplied by the occluded MCA showed excesses in water content, increases in sodium, and decreases in potassium as early as 3 to 4 hours after occlusion. Hemispheric swelling became apparent after 4 to 5 hours, with obvious “gray matter edema.” However, only minimal to moderate increases in the water content of the subcortical white matter (without change in electrolytes) were observed in the same brain sections. Subcortical white matter samples from the affected MCA territory showed gradual increases in water content at 12, 24, and 48 hours, but definite increases in sodium and decreases in potassium were not observed until 24 to 48 hours of ischemia. During this late phase, the “gray matter edema” remained unchanged or underwent partial resolution. Our results agree with data derived from morphological studies suggesting that ischemic cerebral edema develops in a diphasic fashion, with a primary phase of early “gray matter edema” evolving to a secondary phase of late “white matter edema.”