Abstract
To assess the direct cerebrovascular effects of clonidine, we investigated the pharmacological responses of pial vessels to its topical and i.v. administration using a cranial window. Forty-six dogs anesthetized with pentobarbital had the cranial window implanted. We administered six different concentrations of clonidine (10(-8), 10(-7), 10(-6), 10(-5), 10(-4), 10(-3) mol/L) dissolved in artificial cerebrospinal fluid under the window and measured the pial arterial and venous diameters. After pretreating pial vessels with either yohimbine, an alpha2-adrenoceptor antagonist, or glibenclamide, an adenosine triphosphate-sensitive K+-channel blocker, their action was examined after applying clonidine. We also evaluated the effects of i.v. clonidine (5 microg/kg) on pial vascular tone. Topical clonidine produced significant constriction of the pial large and small arteries and veins in a concentration-dependent manner (P < 0.05). Yohimbine abolished the clonidine-induced pial arterial (large P < 0.005; small P < 0.0005) and venous constriction (large and small P < 0.0001). Glibenclamide potentiated the clonidine-induced pial arterial constriction (P < 0.05). I.v. clonidine did not cause significant changes in pial arteries, but it c...Continue Reading
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