Source:http://linkedlifedata.com/resource/pubmed/id/10526121
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1999-11-19
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pubmed:abstractText |
The present study was designed to determine if hyperoxia elicits pial artery vasoconstriction and to characterize the contribution of endothelin-1 (ET-1) to that vascular response in newborn pigs equipped with a closed cranial window. Hyperoxic conditions were established by ventilating the piglets with 100% O(2) during normocapnia and concomitantly topically applying artificial CSF that had been bubbled with 100% O(2). Hyperoxia elevated CSF ET-1 from 23+/-1 to 45+/-4 pg/ml. Hyperoxia also elicited pial artery vasoconstriction that was attenuated by BQ123 (10(-6) M), an ET-1 antagonist (-15+/-1 vs. -5+/-1%). These data indicate that ET-1 contributes to hyperoxic pial artery vasoconstriction.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
18
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pubmed:volume |
842
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
252-5
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10526121-Animals,
pubmed-meshheading:10526121-Arterioles,
pubmed-meshheading:10526121-Blood Pressure,
pubmed-meshheading:10526121-Carbon Dioxide,
pubmed-meshheading:10526121-Cerebral Arteries,
pubmed-meshheading:10526121-Endothelin-1,
pubmed-meshheading:10526121-Female,
pubmed-meshheading:10526121-Hyperoxia,
pubmed-meshheading:10526121-Male,
pubmed-meshheading:10526121-Swine,
pubmed-meshheading:10526121-Vasoconstriction
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pubmed:year |
1999
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pubmed:articleTitle |
Endothelin-1 contributes to normocapnic hyperoxic pial artery vasoconstriction.
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pubmed:affiliation |
Departments of Anesthesia and Pharmacology, University of Pennsylvania and The Children's Hospital of Philadelphia, 34th and Civic Center Blvd., Philadelphia, PA 19104, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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