The role of hydrostatic pressure in ischemic brain edema

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Abstract
The mechanisms responsible for early prenecrotic ischemic brain edema were investigated in rats by comparing brain metabolism, tissue water (HOH) content, and sodium and potassium ion concentration in brain during ischemia induced by decapitation, by the Pulsinelli-Brierley technique, and by carotid embolization. Although brain metabolic functions were similarly disturbed in all three groups, an increase in brain HOH occurred only in the embolism model, which allowed collateral perfusion. Early ischemic brain edema is therefore dependent upon (1) impaired energy-dependent ion pumps and (2) a hydrostatic pressure gradient from patent vascular lumens. Elevated perfusion pressure increases the extent of this early edema. Induced hypertension causes impairment of blood-brain barrier function, as evidenced by extravasation of Evans blue dye 5 minutes after embolic ischemia, and strikingly increases the extent of macromolecular extravasation 4 hours after ictus. This increased protein leakage is accompanied by elevated HOH content and sodium concentration, as compared to findings in normotensive animals. It is concluded that the use of induced hypertension as a therapeutic modality in patients with acute stroke may be harmful.