Pathophysiological Aspects of Blood-Brain Barrier Disturbances in Experimental Brain Tumors and Brain Abscesses

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Abstract
According to the general neuropathological understanding, the breakdown of the blood-brain barrier results in the formation of vasogenic type of brain edema(1). In the early literature, vasogenic brain edema was considered to be essentially a filtrate of blood serum but later emphasis has been placed on the observation that breakdown of barrier function is selective, and that the kinetics of transvascular passage of various blood constituents may differ considerably under different experimental conditions (1–3). Another aspect which has found increasing interest over the past years is the effect of edema fluid on function and metabolism of brain parenchyma. Changes in the composition of the extracellular milieu result in disturbances of intra-extracellular homoiostasis (4), compression of microvasculature by edema fluid or the increase of intercapillary diffusion distance may result in tissue hypoxia (5,6), and cellular uptake of extravasated serum proteins may induce reactive changes of the cell elements involved (7) . In the present investigation, some of these factors are discussed in two models of vasogenic brain edema: edema associated with experimental tumors, and edema associated with experimental abscesses.