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2-Adrenergic Function in Raynaud's Disease

Robert R. Freedman, PhD
Detroit, Mich

Arch Intern Med. 1992;152(9):1929-1933.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 ₂-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 ₂ 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 . . . [Full Text PDF of this Article]

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