• A Salvucci and W M Armstead.
• Department of Anesthesia, University of Pennsylvania, Philadelphia, PA 19104, USA.
• Brain Res. 2000 Dec 29; 887 (2): 406-12.

AbstractThis study was designed to characterize the role of vasopressin in impaired pial artery dilation to activators of the ATP sensitive K (K(ATP)) and calcium sensitive K (K(ca)) channel following fluid percussion brain injury (FPI) in newborn pigs equipped with a closed cranial window. Topical vasopressin was coadministered with the K(ATP) and K(ca) 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-(beta-mercapto-beta, beta-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 K(ATP) and K(ca) channel mediated cerebrovasodilation. These data suggest that vasopressin contributes to impaired K(ATP) and K(ca) channel function after brain injury.

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