| Mechanisms of protection of the blood-brain barrier during acute hypertension in chronically hypertensive rats. | |
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MedLine Citation:
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PMID: 3596775 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Spontaneously hypertensive rats are less susceptible than normotensive rats to disruption of the blood-brain barrier during acute hypertension. The purpose of this study was to examine mechanisms that protect the blood-brain barrier from disruption in chronically hypertensive rats during acute hypertension. Normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were studied using intravital fluorescent microscopy and fluorescein-labeled dextran. Disruption of the blood-brain barrier was characterized by the appearance of microvascular leaky sites and quantitated by the clearance of fluorescein-labeled dextran. We measured pressure (servo null) in pial arterioles and venules 40 to 60 micron in diameter. In WKY, acute, phenylephrine-induced hypertension increased pial arteriolar pressure by 47 +/- 7 mm Hg (mean +/- SE) and pial venous pressure by 20 +/- 2 mm Hg. Leaky sites increased from 0 to 28 +/- 2. In SHRSP, acute hypertension increased pial arteriolar pressure 44 +/- 8 mm Hg, but pial venous pressure increased only 6 +/- 1 mm Hg and leaky sites increased from 0 to only 6 +/- 1. All leaky sites were venular. In another group of WKY and SHRSP, we increased pial venous pressure passively with a neck cuff. In WKY, venous pressure increased by 22 +/- 2 mm Hg, and leaky sites increased from 0 to 23 +/- 2. In SHRSP, venous pressure increased by 19 +/- 1 mm Hg, and leaky sites increased from 0 to 24 +/- 2. Thus, when venous pressure is increased to the same level in WKY and SHRSP, disruption of the blood-brain barrier is similar. We conclude that protection of the blood-brain barrier during acute hypertension in SHRSP is related to attenuation of increases in pial venous pressure, not pial arteriolar pressure, and the blood-brain barrier in venules of SHRSP probably is not inherently resistant to disruption. |
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Authors:
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W G Mayhan; F M Faraci; D D Heistad |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Hypertension Volume: 9 ISSN: 0194-911X ISO Abbreviation: Hypertension Publication Date: 1987 Jun |
Date Detail:
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Created Date: 1987-08-05 Completed Date: 1987-08-05 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: III101-5 Citation Subset: IM |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Disease Animals Aorta / physiopathology Biomechanics Blood Pressure Blood-Brain Barrier* Capillary Permeability Constriction, Pathologic Hypertension / physiopathology* Male Neck / blood supply Pia Mater / blood supply Rats Rats, Inbred SHR Rats, Inbred WKY Venous Pressure Venules / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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HL 14388/HL/NHLBI NIH HHS; HL 35940/HL/NHLBI NIH HHS; HL 7180/HL/NHLBI NIH HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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