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- W2978003485 abstract "Cerebral hypoxia/ischemia (H/I) impairs cerebrovasodilation in response to hypercapnia and hypotension in the newborn pig, exogenous uPA potentiates this effect, while blockade of endogenous uPA-mediated vasoactivity prevents it completely. This study investigated the role of integrin αVβ3, in uPA-mediated impairment of cerebrovasodilation after H/I in piglets equipped with a closed cranial window. Pial artery dilation induced by hypercapnia (pCO2 75 mm Hg) and hypotension (mean arterial blood pressure decreased by 45%) was blunted after H/I, reversed to vasconstriction in piglets treated with uPA (10−7 M), a concentration observed in CSF after H/I, but reverted to dilation no different than pre-insult in piglets administered an anti αVβ3 antibody (10 ng/ml) in addition to uPA (26 ± 1, 9 ± 1, -10 ± 3, and 22 ± 3 % for hypercapnia before H/I, after H/I, after H/I with uPA, and after H/I with combined uPA and anti-αVβ3 antibody). Responses to isoproterenol were unchanged after H/I and combined uPA and anti αVβ3 antibody. Similar results were obtained for combined administration of uPA with the αVβ3 antagonist cRGDfV and RGDS, but not for the inactive analogue, RGDES. These data show that activation of the integrin αVβ3 contributes to uPA- mediated impairment of pial artery dilation after H/I. These data suggest that inhibition of uPA and integrin signaling may preserve cerebrohemodynamic control after H/I." @default.
- W2978003485 created "2019-10-10" @default.
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- W2978003485 date "2009-04-01" @default.
- W2978003485 modified "2023-10-16" @default.
- W2978003485 title "Inhibition of integrin aVB3 prevents uPA–mediated impairment of cerebrovasodilation after cerebral hypoxia/ischemia" @default.
- W2978003485 doi "https://doi.org/10.1096/fasebj.23.1_supplement.613.5" @default.
- W2978003485 hasPublicationYear "2009" @default.
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