| pubmed-article:16256083 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0917798 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0038050 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0002932 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0018549 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C1955862 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0205234 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0392760 | lld:lifeskim |
| pubmed-article:16256083 | lifeskim:mentions | umls-concept:C0205374 | lld:lifeskim |
| pubmed-article:16256083 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:16256083 | pubmed:dateCreated | 2005-11-18 | lld:pubmed |
| pubmed-article:16256083 | 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. | lld:pubmed |
| pubmed-article:16256083 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16256083 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16256083 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16256083 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16256083 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16256083 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16256083 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16256083 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16256083 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16256083 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16256083 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16256083 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:16256083 | pubmed:issn | 0006-8993 | lld:pubmed |
| pubmed-article:16256083 | pubmed:author | pubmed-author:ShimizuKatsuy... | lld:pubmed |
| pubmed-article:16256083 | pubmed:author | pubmed-author:BusijaDavid... | lld:pubmed |
| pubmed-article:16256083 | pubmed:author | pubmed-author:HoriguchiTaka... | lld:pubmed |
| pubmed-article:16256083 | pubmed:author | pubmed-author:RajapakseNish... | lld:pubmed |
| pubmed-article:16256083 | pubmed:author | pubmed-author:KisBelaB | lld:pubmed |
| pubmed-article:16256083 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16256083 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:16256083 | pubmed:volume | 1062 | lld:pubmed |
| pubmed-article:16256083 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16256083 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16256083 | pubmed:pagination | 127-33 | lld:pubmed |
| pubmed-article:16256083 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:16256083 | pubmed:meshHeading | pubmed-meshheading:16256083... | lld:pubmed |
| pubmed-article:16256083 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16256083 | 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. | lld:pubmed |
| pubmed-article:16256083 | pubmed:affiliation | Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, NC 27157-1083, USA. | lld:pubmed |
| pubmed-article:16256083 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16256083 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:16256083 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16256083 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16256083 | lld:pubmed |
