Abstract

The authors present the results of an investigation studying the resolution of vasogenic brain edema using cold injury in cats. The appearance of RISA-I131 and sucrose-C14 lebeled edema fluid in the ventricular cerebrospinal fluid (CSF) was assessed by means of ventriculocisternal perfusion. The effect of low- or high-pressure perfusion on edema spread was determined by measuring the water, sodium, RISA-I131, and sucrose-C14 content of serial tissue blocks taken from the injured cortex through the white matter to the ventricular ependyma. The findings indicate that increasing the hydrostatic pressure gradient between edematous brain and CSF enhances the clearance of edema fluid into the ventricular CSF. This was conclusively demonstrated with low-pressure ventricular perfusion which markedly diminished the amount of edema close to the ventricles compared to the controls. The concentration of albumin, sodium, and potassium to the fluid removed from the tissue during low-pressure perfusion indicates that bulk flow was the primary method of edema movement through the extracellular space. With high-pressure perfusion the concentration profiles suggested alternative mechanisms of edema resolution, such as diffusion and reabsorption into capillaries.

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