The effects of clonidine on human digital vasculature

Large concentrations of alpha(2) agonists cause vasoconstriction. However, the threshold of the vasoconstrictive effect in humans is not known. We stu died 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 wa s continuously monitored via radial arterial catheter and vasoconstriction via finger volume plethysmography measuring infrared light transmitted thro ugh a fingertip (LTF). Clonidine was administered, targeting plasma clonidi ne 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 subj ects, clonidine (2.25 ng/mL) decreased LTF by 14% +/- 13% and SEP 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 SEP from 91 +/- 7 to 106 +/- 19 mm Hg (P < 0.0001). We conclude that the same dose of cloni dine that decreased blood pressure and caused vasodilation in awake subject s had the opposite effect in anesthetized subjects with reduced sympathetic tone, increasing blood pressure and causing vasoconstriction in human digi tal vasculature. Our findings suggest that the lower threshold for clonidin e-induced vasoconstriction in human digital vasculature is 1.0 ng/mL.