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Botulinum toxin abolishes sweating via impaired sweat gland responsiveness to exogenous acetylcholine
Author(s) -
Shibasaki M.,
Davis S.L.,
Cui J.,
Low D.A.,
Keller D.M.,
Crandall C.G.
Publication year - 2009
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2009.09248.x
Subject(s) - medicine , library science , gerontology , computer science
Summary Background Botulinum toxin A (BTX) disrupts neurotransmitter release from cholinergic nerves. The effective duration of impaired sweat secretion with BTX is longer relative to that of impaired muscle contraction, suggesting different mechanisms in these tissues. Objectives The aim of this study was to test the hypothesis that BTX is capable of altering sweating by reducing the responsiveness of the sweat gland to acetylcholine. Methods BTX was injected into the dorsal forearm skin of healthy subjects at least 3 days before subsequent assessment. On the day of the experiment, intradermal microdialysis probes were placed within the BTX‐treated area and in an adjacent untreated area. Incremental doses of acetylcholine were administered through the microdialysis membranes while the sweat rate (protocol 1; n = 8) or a combination of sweat rate and skin blood flow (protocol 2; n = 8) were assessed. Results A relative absence of sweating was observed at the BTX site for both protocols (protocol 1: 0·05 ± 0·09 mg cm −2 min −1 ; protocol 2: 0·03 ± 0·04 mg cm −2 min −1 , both at the highest dose of acetylcholine), while the sweat rate increased appropriately at the control sites (protocol 1: 0·90 ± 0·46 mg cm −2 min −1 ; protocol 2: 1·07 ± 0·67 mg cm −2 min −1 ). Cutaneous vascular conductance increased to a similar level at both the BTX and control sites. Conclusions These results demonstrate that BTX is capable of inhibiting sweat secretion by reducing the responsiveness of the sweat gland to acetylcholine, while not altering acetylcholine‐mediated cutaneous vasodilatation.