Linked Life Data

16256083

Source:http://linkedlifedata.com/resource/pubmed/id/16256083

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2005-11-18
pubmed:abstractText
We investigated the participation of ATP-sensitive potassium (K(ATP)) channels, adenosine A1 receptors, and the effects of different levels of halothane anesthesia in the development of CSD-induced ischemic tolerance. To elicit CSD, 0.5 M KCl was applied for 2 h to the right hemisphere of halothane anesthetized male Wistar rats. The inhalation concentration of halothane during CSD was maintained at 0.5% (n = 8), 1.0% (n = 8), or 2.0% (n = 8). For control animals, saline was applied instead of KCl (n = 8). To inhibit K(ATP) channels or adenosine A1 receptors, glibenclamide (0.1 mg/kg icv; n = 8), 5-hydroxydeconaoate (5-HD; 100 mg/kg ip; n = 12), or 8-Cyclopentyl-1, 3-dipropylxanthine (DPCPX) (1.0 mg/kg ip; n = 8) was applied before preconditioning during 1.0% halothane anesthesia. Temporary occlusion (120 min) of the right middle cerebral artery was induced 4 days after preconditioning and the infarct volume was measured. Preconditioning elicited under 1.0% halothane reduced cortical infarct volume from 277 +/- 15 mm3 in the control group to 159 +/- 14 mm3 in the CSD group (mean +/- SEM, P < 0.05). In contrast, CSD induced during inhalation of 0.5% or 2.0% halothane did not confer ischemic tolerance. The reduction in infarct area with CSD during inhalation of 1% halothane was not changed in animals treated with glibenclamide or 5-HD or DPCPX. These results uncover a crucial role of halothane level but not of K(ATP) channels or adenosine A1 receptors in the preconditioning effects of CSD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
1062
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
127-33
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16256083-ATP-Binding Cassette Transporters, pubmed-meshheading:16256083-Adenosine A1 Receptor Antagonists, pubmed-meshheading:16256083-Anesthetics, Inhalation, pubmed-meshheading:16256083-Animals, pubmed-meshheading:16256083-Brain, pubmed-meshheading:16256083-Cortical Spreading Depression, pubmed-meshheading:16256083-Dose-Response Relationship, Drug, pubmed-meshheading:16256083-Halothane, pubmed-meshheading:16256083-Ischemic Attack, Transient, pubmed-meshheading:16256083-Ischemic Preconditioning, pubmed-meshheading:16256083-Male, pubmed-meshheading:16256083-Potassium Channel Blockers, pubmed-meshheading:16256083-Potassium Channels, Inwardly Rectifying, pubmed-meshheading:16256083-Rats, pubmed-meshheading:16256083-Rats, Wistar, pubmed-meshheading:16256083-Receptor, Adenosine A1
pubmed:year
2005
pubmed:articleTitle
Cortical spreading depression (CSD)-induced tolerance to transient focal cerebral ischemia in halothane anesthetized rats is affected by anesthetic level but not ATP-sensitive potassium channels.
pubmed:affiliation
Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC 27157-1083, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural