| pubmed-article:15908467 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15908467 | lifeskim:mentions | umls-concept:C0270611 | lld:lifeskim |
| pubmed-article:15908467 | lifeskim:mentions | umls-concept:C0018850 | lld:lifeskim |
| pubmed-article:15908467 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:15908467 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:15908467 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:15908467 | pubmed:dateCreated | 2005-8-15 | lld:pubmed |
| pubmed-article:15908467 | pubmed:abstractText | Fluid percussion brain injury (FPI) impairs pial artery dilation to activators of the ATP-sensitive (K(ATP)) and calcium-activated (K(Ca)) K(+) channels. This study investigated the role of heat shock protein (HSP) in the modulation of K(+) channel-induced pial artery dilation after FPI in newborn pigs equipped with a closed cranial window. Under nonbrain injury conditions, topical coadministration of exogenous HSP-27 (1 mug/ml) blunted dilation to cromakalim, CGRP, and NS-1619 (10(-8) and 10(-6) M; cromakalim and CGRP are K(ATP) agonists and NS-1619 is a K(Ca) agonist). In contrast, coadministration of exogenous HSP-70 (1 mug/ml) potentiated dilation to cromakalim, CGRP, and NS-1619. FPI increased the cerebrospinal fluid (CSF) concentration of HSP-27 from 0.051 +/- 0.012 to 0.113 +/- 0.035 ng/ml but decreased the CSF concentration of HSP-70 from 50.42 +/- 8.96 to 30.9 +/- 9.9 ng/ml at 1 h postinsult. Pretreatment with topical exogenous HSP-70 (1 mug/ml) before FPI fully blocked injury-induced impairment of cromakalim and CGRP dilation and partially blocked injury-induced impairment of dilation to NS-1619. These data indicate that HSP-27 and HSP-70 contribute to modulation of K(+) channel-induced pial artery dilation. These data suggest that HSP-70 is an endogenous protectant of which its actions may be unmasked and/or potentiated with exogenous administration before brain injury. | lld:pubmed |
| pubmed-article:15908467 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15908467 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15908467 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15908467 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15908467 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15908467 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15908467 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15908467 | pubmed:issn | 0363-6135 | lld:pubmed |
| pubmed-article:15908467 | pubmed:author | pubmed-author:ArmsteadWilli... | lld:pubmed |
| pubmed-article:15908467 | pubmed:author | pubmed-author:HeckerJames... | lld:pubmed |
| pubmed-article:15908467 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15908467 | pubmed:volume | 289 | lld:pubmed |
| pubmed-article:15908467 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15908467 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15908467 | pubmed:pagination | H1184-90 | lld:pubmed |
| pubmed-article:15908467 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:15908467 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15908467 | pubmed:articleTitle | Heat shock protein modulation of KATP and KCa channel cerebrovasodilation after brain injury. | lld:pubmed |
| pubmed-article:15908467 | pubmed:affiliation | Department of Anesthesia, University of Pennsylvania, 3620 Hamilton Walk, Rm. 305 John Morgan, Philadelphia, PA 19104, USA. armsteaw@uphs.upenn.edu | lld:pubmed |
| pubmed-article:15908467 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15908467 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15908467 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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