Pathophysiological aspects of blood-brain barrier disturbances in experimental brain tumors and brain abscesses.

Experimental tumors and abscesses were produced by intrahemispheric inoculation of a blastomatous glial cell clone and of staphylococcus aureus, respectively. In both models severe vasogenic brain edema developed. The site of the barrier lesion was identified by systemic application of Evans blue or peroxidase, and the spread of edema by immunoautoradiographic localisation of extravasated serum proteins. In both experimental conditions, serum proteins accumulated diffusely in the white matter of the ipsilateral hemisphere, although the barrier lesion was strictly confined to the pathological focus. Water content of the edematous white matter in the vicinity of tumors and abscesses increased from 69.1 to 80.6 and 82.3 ml/100g w.w., respectively. This increase was associated with a volume-dependent decrease of flow, a parallel increase of sodium and an increase of extravasated serum proteins. The latter was determined by a newly developed immunochemical approach with appropriate corrections for the intravascular fraction of total serum protein content. The calculated concentration of sodium in edema fluid of tumors and abscesses amounted to 132 and 129 ueq/ml, respectively. The concentration of serum proteins was 8.7 and 6.4 mg/ml, respectively. Protein content of edema fluid, in consequence was less than 10% of blood serum. This suggests that fluid accumulation in vasogenic edema cannot be explained by the oncotic properties of extravasated proteins alone.