Add time:08/08/2019         Source:sciencedirect.com

This study was designed to characterize the role of vasopressin in impaired pial artery dilation to activators of the ATP sensitive K (KATP) and calcium sensitive K (Kca) channel following fluid percussion brain injury (FPI) in newborn pigs equipped with a closed cranial window. Topical vasopressin was coadministered with the KATP and Kca channel agonists cromakalim and NS1619 in a concentration approximating that observed in CSF following FPI. Vasopressin so administered attenuated pial artery dilation to these K+ channel activators under conditions of equivalent baseline diameter during non injury conditions (13±1 and 23±1 vs. 4±1 and 10±2% for cromakalim 10−8, 10−6 M before and after vasopressin, respectively). Attenuated responses were fully restored when these agonists were coadministered with vasopressin and the vasopressin antagonist [l-(β-mercapto-β,β-cyclopentamethylene propionic acid) 2-(o-methyl)-Tyr-AVP] (MEAVP). Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI and MEAVP preadministration partially prevented such impairment (13±1 and 23±1, sham control; 2±1 and 5±1, FPI; and 9±1 and 15±2%, FPI-MEAVP pretreated for responses to cromakalim 10−8, 10−6 M, respectively). These data show that vasopressin blunts KATP and Kca channel mediated cerebrovasodilation. These data suggest that vasopressin contributes to impaired KATP and Kca channel function after brain injury.

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