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a2-Adrenergic Function in Raynaud's Disease

Robert R. Freedman, PhD
Arch Intern Med. 1992;152(9):1929-1933. doi:10.1001/archinte.1992.00400210147031.
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To the Editor.—  I read with interest the recent review article on Raynaud's phenomenon by Klippel.1 The author correctly states that we were able to provoke cold-induced vasospastic attacks in patients with primary Raynaud's disease whose digital nerves had been blocked by lidocaine.2 However, Klippel's account of our findings on α2-adrenergic function in Raynaud's disease is incorrect. We performed brachial artery infusions of clonidine hydrochloride (0.25 to 4.0 μg/min) in eight patients with Raynaud's disease and in 11 normal volunteers.3 Patients with Raynaud's disease had significantly greater vasoconstriction than did control subjects at all doses that were administered. These findings were independently replicated.4 Lindblad et al5 delivered an α2 agonist by iontophoresis, which perfused only a small area of skin and cannot assure accurate drug delivery.5 In contrast, we3 and others4 administered clonidine hydrochloride by pump through the brachial


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