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The Effects of Clonidine on Human Digital Vasculature

2000; Lippincott Williams & Wilkins; Volume: 91; Issue: 4 Linguagem: Inglês

10.1097/00000539-200010000-00006

1526-7598

Pekka Talke, James E. Caldwell, Charles A. Richardson, Tom Heier,

Veterinary Pharmacology and Anesthesia

Large concentrations of α2 agonists cause vasoconstriction. However, the threshold of the vasoconstrictive effect in humans is not known. We studied seven volunteers to determine the lower limit of the vasoconstrictive effect of clonidine. Subjects were studied while they were awake, and they were anesthetized with propofol/alfentanil/N2O. Arterial blood pressure was continuously monitored via radial arterial catheter and vasoconstriction via finger volume plethysmography measuring infrared light transmitted through a fingertip (LTF). Clonidine was administered, targeting plasma clonidine concentrations of 0.3, 0.45, 0.68, 1.0, 1.5, and 2.25 ng/mL. The maximum change from preclonidine values for systolic blood pressure (SBP) and LTF was analyzed by using repeated measures analysis of variance. In awake subjects, clonidine (2.25 ng/mL) decreased LTF by 14% ± 13% and SBP from 141 ± 7 to 110 ± 15 mm Hg (P < 0.0001). In contrast, clonidine (2.25 ng/mL) increased LTF in anesthetized subjects by 21% ± 16% and SBP from 91 ± 7 to 106 ± 19 mm Hg (P < 0.0001). We conclude that the same dose of clonidine that decreased blood pressure and caused vasodilation in awake subjects had the opposite effect in anesthetized subjects with reduced sympathetic tone, increasing blood pressure and causing vasoconstriction in human digital vasculature. Our findings suggest that the lower threshold for clonidine-induced vasoconstriction in human digital vasculature is 1.0 ng/mL. Implications At clinically relevant doses, clonidine produced vasoconstriction in digital vasculature and increased blood pressure in anesthetized volunteers, while producing the opposite effect in the awake state.