Alterations of Membrane-Bound Enzymes in Vasogenic Edema

Abstract

In recent years some of the pathophysiological mechanisms of vasogenic edema have been thoroughly studied and recognized, such as the initial breakdown of the blood-brain barrier, the exudation into the extracellular space of plasma fluid according to pressure gradients, the resolution by drainage into the ventricle, and/or uptake of proteins by astrocytes. Yet this type of edema should not only be considered as a simple extracellular event depending on physical forces. Soon after the onset of extracellular edema intra-cellular accumulation of fluid occurs, mainly in astrocytes and neuronal dendrites^11,2. This intracellular component of vasogenic edema is poorly understood. Since rCBF is reduced in edematous lesions, cellular swelling has been considered to be the consequence of energy failure from lack of O₂ and substrates. Some workers have reported a breakdown of energy reserves concomitant to a decrease of rCBF^12,7. But in similar models, O₂ supply has been found to be essentially normal⁸ and several authors have reported normal levels of high-energy compounds¹⁶.