{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T18:40:12Z","timestamp":1774464012869,"version":"3.50.1"},"reference-count":50,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2005,9]]},"abstract":"<jats:p>Fluid percussion brain injury (FPI) impairs pial artery dilation to activators of the ATP-sensitive (K<jats:sub>ATP<\/jats:sub>) and calcium-activated (K<jats:sub>Ca<\/jats:sub>) K<jats:sup>+<\/jats:sup>channels. This study investigated the role of heat shock protein (HSP) in the modulation of K<jats:sup>+<\/jats:sup>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 \u03bcg\/ml) blunted dilation to cromakalim, CGRP, and NS-1619 (10<jats:sup>\u22128<\/jats:sup>and 10<jats:sup>\u22126<\/jats:sup>M; cromakalim and CGRP are K<jats:sub>ATP<\/jats:sub>agonists and NS-1619 is a K<jats:sub>Ca<\/jats:sub>agonist). In contrast, coadministration of exogenous HSP-70 (1 \u03bcg\/ml) potentiated dilation to cromakalim, CGRP, and NS-1619. FPI increased the cerebrospinal fluid (CSF) concentration of HSP-27 from 0.051 \u00b1 0.012 to 0.113 \u00b1 0.035 ng\/ml but decreased the CSF concentration of HSP-70 from 50.42 \u00b1 8.96 to 30.9 \u00b1 9.9 ng\/ml at 1 h postinsult. Pretreatment with topical exogenous HSP-70 (1 \u03bcg\/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<jats:sup>+<\/jats:sup>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.<\/jats:p>","DOI":"10.1152\/ajpheart.00276.2005","type":"journal-article","created":{"date-parts":[[2005,5,21]],"date-time":"2005-05-21T00:24:22Z","timestamp":1116635062000},"page":"H1184-H1190","source":"Crossref","is-referenced-by-count":16,"title":["Heat shock protein modulation of K<sub>ATP<\/sub>and K<sub>Ca<\/sub>channel cerebrovasodilation after brain injury"],"prefix":"10.1152","volume":"289","author":[{"given":"William M.","family":"Armstead","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James 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