Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-8-15
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
289
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1184-90
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15908467-Animals, pubmed-meshheading:15908467-Animals, Newborn, pubmed-meshheading:15908467-Benzimidazoles, pubmed-meshheading:15908467-Blood Pressure, pubmed-meshheading:15908467-Brain Injuries, pubmed-meshheading:15908467-Calcitonin Gene-Related Peptide, pubmed-meshheading:15908467-Calcium Channels, pubmed-meshheading:15908467-Cerebrovascular Circulation, pubmed-meshheading:15908467-Cromakalim, pubmed-meshheading:15908467-Female, pubmed-meshheading:15908467-HSP70 Heat-Shock Proteins, pubmed-meshheading:15908467-Heat-Shock Proteins, pubmed-meshheading:15908467-Male, pubmed-meshheading:15908467-Pia Mater, pubmed-meshheading:15908467-Potassium Channels, pubmed-meshheading:15908467-Swine, pubmed-meshheading:15908467-Vasodilation, pubmed-meshheading:15908467-Vasodilator Agents
pubmed:year
2005
pubmed:articleTitle
Heat shock protein modulation of KATP and KCa channel cerebrovasodilation after brain injury.
pubmed:affiliation
Department of Anesthesia, University of Pennsylvania, 3620 Hamilton Walk, Rm. 305 John Morgan, Philadelphia, PA 19104, USA. armsteaw@uphs.upenn.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural