AJP - Regu Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 247: R634-R638, 1984;
0363-6119/84 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ziylan, Y. Z.
Right arrow Articles by Rapoport, S. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ziylan, Y. Z.
Right arrow Articles by Rapoport, S. I.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 247, Issue 4 634-R638, Copyright © 1984 by American Physiological Society

ARTICLES

Blood-brain barrier permeability to sucrose and dextran after osmotic opening

Y. Z. Ziylan, P. J. Robinson and S. I. Rapoport

Regional cerebrovascular permeability-surface area (PA) products were calculated for two nonelectrolyte tracers differing considerably in molecular weight and size [( 14C]sucrose: mol wt 340 daltons, radius 5 A; and [3H]dextran: mol wt approximately 79,000 daltons, radius approximately 65 A) in control (uninfused) rats and in rats 6, 35, and 55 min after the blood-brain barrier was opened by a 30-s infusion of 1.8 molal L(+)-arabinose into a carotid artery. In control brain regions, mean PA for [14C]sucrose was 10(-5) s-1, whereas PA was not measurable for [3H]dextran. Six minutes after arabinose infusion, PA for both substances increased dramatically to 10(-4) s-1 or more; PA then declined at 35 and 55 min after arabinose infusion, but more markedly for [3H]dextran than for [14C]sucrose. The results demonstrate a size-dependent, differential rate of closure of the blood-brain barrier after osmotic opening. This is shown to be consistent with a pore model with bulk flow for blood-brain barrier permeability after osmotic opening.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
W. A. Banks
The dam breaks: disruption of the blood-brain barrier in diabetes mellitus
Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2595 - H2596.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
J. D. Huber, R. L. VanGilder, and K. A. Houser
Streptozotocin-induced diabetes progressively increases blood-brain barrier permeability in specific brain regions in rats
Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2660 - H2668.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
B. S. Stonestreet, G. B. Sadowska, J. Leeman, R. C. Hanumara, K. H. Petersson, and C. S. Patlak
Effects of acute hyperosmolality on blood-brain barrier function in ovine fetuses and lambs
Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2006; 291(4): R1031 - R1039.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online