The goal of this study was to determine whether increases in cerebral venous pressure contribute to, and may account for, disruption of the blood-brain barrier during acute hypertension and hyperosmolar stimuli. We studied the relation between pial venous pressure and disruption of the blood-brain barrier during acute arterial hypertension, superior venae cavae occlusion, and superfusion with hyperosmolar arabinose. Sprague-Dawley rats were studied using intravital fluorescent microscopy and fluorescein-labelled dextran (mol. wt. = 70,000). Disruption of the blood-brain barrier was characterized by the appearance of microvascular leaky sites and quantitated by the clearance of fluorescein dextran. We measured pressure (servo null) in pial arterioles and venules 40-60 μm in diameter. Acute hypertension, occlusion of the superior venae cavae, and hyperosmolar arabinose produced leaky sites primarily in venules. Acute hypertension increased arteriolar pressure and also venular pressure, from 7 ± 1 (mean ± SE) to 28 ± 2 mm Hg. Clearance of fluorescein dextran increased from 0.03 ± 0.01 to 2.90 ± 0.40 ml/sec x 10-6. Occlusion of the superior venae cavae increased pial venous pressure from 7 ± 1 to 30 ± 3 mm Hg, and clearance of fluorescein dextran, from 0.02 ± 0.01 to 3.10 ± 0.59 ml/sec x 10-6. In contrast to acute hypertension, there was a decrease in arterial and pial arteriolar pressure during occlusion of the superior venae cavae. Thus, similar increases in venous pressure during acute hypertension and superior venae cavae occlusion, despite directionally opposite changes in arterial and arteriolar pressure, produced similar disruption of the blood-brain barrier. Disruption of the blood-brain barrier during hyperosmolar arabinose was not associated with an increase in pial venous pressure. The findings suggest that 1) increases in pial venous pressure during acute hypertension are of sufficient magnitude to account for disruption of the blood-brain barrier, and 2) disruption of the blood-brain barrier during hyperosmolar arabinose is not associated with increases in pial venous pressure.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine