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Am J Physiol Heart Circ Physiol (May 20, 2005). doi:10.1152/ajpheart.00276.2005
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Submitted on March 21, 2005
Accepted on May 11, 2005

Heat Shock Protein Modulation Of KATP And Kca Channel Cerebrovasodilation After Brain Injury

William M Armstead1* and James G Hecker2

1 Anesthesia, University of Pennsylvania, Philadelphia, PA, USA; Anesthesia, University of Pennsylvania, Philadelphia, PA, USA
2 Anesthesia, University of Pennsylvania, Philadelphia, PA, USA; Pharmacology, University of Pennsylvania, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: armsteaw{at}uphs.upenn.edu.

Fluid percussion brain injury (FPI) impairs pial artery dilation to activators of the ATP sensitive (KATP) and calcium activated (Kca) channel. 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 non brain injury conditions, topical co-administration of exogenous HSP 27 (1 µg/ml) blunted dilation to cromakalim, calcitonin gene related peptide (CGRP), and NS 1619 (10-8, 10-6 M) (KATP and Kca agonists respectively). In contrast, co-administration of exogenous HSP 70 (1 µg/ml) potentiated dilation to cromakalim, CGRP, and NS 1619. FPI increased the 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 hour post insult. Pretreatment with topical exogenous HSP 70 (1 µg/ml) prior to 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 whose actions may be unmasked and/or potentiated with exogenous administration prior to brain injury.




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