[Superacute changes in blood-brain barrier following cerebral venous hypertension due to an embolic occlusion of cerebral venous sinus].

Pathophysiological mechanism of hemorrhagic infarction and brain edema following obliteration of venous outflow tract has been poorly understood. We analyzed a superacute change of the blood-brain barrier in a rat experimental model of venous hypertension produced by an embolic occlusion of superior sagittal sinus (SSS). In all thirty-seven animals received retrograde embolization, marked increments of SSS pressure were noted immediately after embolic occlusion of the sinus. Severity and geographical patterns of the disruption of blood-brain barrier were then analyzed photomicrographically, visualized by the autofluorescence of the exuded Evans blue with Hematoxylin-eosin stain. Relationship between the degree of SSS pressure increment and the severity of the blood-brain barrier destruction was studied. In ten out of the seventeen animals (59%), analyzed five minutes after embolization, exudation of the dye was demonstrated. The degree of SSS pressure increment in the animals with dye exudation was higher than in the animals without them. In five out of the nine animals (56%), analyzed fifteen minutes after embolization, exudation of the dye was also demonstrated. The degree of SSS pressure increments in the animals with dye exudation was statistically higher than those in the non-exuded ones. Especially, all the animals with SSS pressure higher than 75 mmHg were associated with severe exudation of the dye. The exudation of the dye was more prominent in the white matter than in the cortical gray matter. Following pathological analysis have revealed that exudation of the dye was most prominent around the capillary and the venule in the white matter. Microvacuolation around these vessels was also noted.(ABSTRACT TRUNCATED AT 250 WORDS)