The purpose of this study was to examine hemodynamic mechanisms of protection of the blood-brain barrier in the brain stem during acute hypertension. We used a new method to examine the microcirculation of the brain stem. Intravital fluorescent microscopy and fluorescein-labeled dextran were used to evaluate disruption of the blood-brain barrier during acute hypertension in rats. During control conditions, pressure (servo null) in arterioles (60 μm in diameter) was 50 ± 2% (mean ± SE) of systemic arterial pressure in the cerebrum and 67 ± 1% of systemic arterial pressure in the brain stem (P < 0.05 vs. cerebrum). In the cerebrum, pial venous pressure increased from 7 ± 1 to 25 ± 2 mmHg during acute hypertension, and there was a marked disruption of the blood-brain barrier in venules (26 ± 2 leaky sites). In contrast, in the brain stem, pial venous pressure increased from 4 ± 1 to only 8 ± 1 mmHg (P < 0.05 vs. cerebrum), and there was minimal disruption of the blood-brain barrier in venules (1.5 ± 0.6 leaky sites, P < 0.05 vs. cerebrum). During acute hypertension, increases in blood flow (microspheres) were less in brain stem than in cerebrum. The findings suggest 1) distribution of vascular resistance differs in the brain stem and cerebrum under control conditions, whereas large arteries account for a greater fraction of resistance in cerebrum; 2) pial venous pressure increases less in brain stem than cerebrum during acute hypertension, so that the blood-brain barrier is protected; and 3) pressure drops significantly more between arterioles and venules in the brain stem than cerebrum during acute hypertension, which suggests that resistance of small vessels is greater in brain stem than cerebrum during acute hypertension.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - 1986|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)