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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2000-11-13
pubmed:abstractText
We investigated the contribution of ATP-sensitive potassium channels (K(ATP)) and calcium-activated potassium channels (Kca2+) to cortical spreading depression (CSD)-associated hyperemia using the rat closed cranial window model. The peak CBF response was enhanced by 12 +/- 5, 13 +/- 4, and 28 +/- 8% (p<0.01) of the control with 10(-6), 10(-5) and 10(-4) mol/l glibenclamide (glyb), a K(ATP) antagonist, respectively. We also calculated the area under the CBF curve to fully represent the extent of hyperemia during CSD. The area increased by 30 +/- 8 (p<0.05), 72 +/- 31 (p<0.05) and 88 +/- 20% (p<0.05) of the control with 10(-6), 10(-5) and 10(-4) mol/l glyb, respectively. However, charybdotoxin (CTX), a Kca2+ antagonist showed no effect. The effect of glyb was inhibited by pretreatment with 5 mg/kg indomethacin. We conclude that activation of K(ATP), perhaps associated with neurons, plays an inhibitory role in the CSD-associated hyperemia via an indomethacin-sensitive mechanism.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0959-4965
pubmed:author
pubmed:issnType
Print
pubmed:day
14
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2103-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Glibenclamide enhances cortical spreading depression-associated hyperemia in the rat.
pubmed:affiliation
Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1083, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.