Objective: Menopausal hot flashes can seriously disrupt the lives of symptomatic women. The physiological mechanisms of the hot flash efferent responses, particularly in the cutaneous circulation, are not completely understood. The aim of this study was to examine the mechanisms of increases in skin blood flow during the postmenopausal hot flash in symptomatic women.
Methods: Healthy postmenopausal women rested in a temperature-controlled laboratory while responses before and during hot flashes were recorded for three unique protocols. In protocols 1 and 2, women were locally pretreated with an intradermal injection of botulinum toxin A (BTX; blocks the release of neurotransmitters from sympathetic cholinergic nerves) in the forearm (protocol 1) and in the glabellar region (protocol 2). In protocol 3, skin sympathetic nerve activity from the peroneal nerve was recorded, along with skin blood flow and sweating within the region innervated by that neural signal. Skin blood flow was indexed using laser-Doppler flowmetry at the BTX-treated and adjacent untreated control sites. The onset of a hot flash was objectively identified as a transient and pronounced increase in sternal sweat rate.
Results: The increases in forearm (protocol 1) and glabellar skin (protocol 2) blood flow during hot flashes were attenuated at the BTX sites relative to the adjacent untreated sites (P < 0.05 for both protocols). In protocol 3, skin sympathetic nerve activity significantly increased during hot flashes and returned to pre-hot flash levels after the hot flashes.
Conclusions: Increases in skin blood flow during postmenopausal hot flashes are neurally mediated primarily through BTX-sensitive nerves, presumably sympathetic cholinergic.
From the 1Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, Dallas, TX; and 2Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, TX.
Received May 3, 2010; revised and accepted August 9, 2010.
David Low is currently affiliated with Neurovascular and Autonomic Unit, St Mary's Hospital Faculty of Medicine, Imperial College of London, England.
Funding/support: This work was supported by grants from the National Institutes of Health National Institute on Aging (AG030189).
Financial disclosure/conflicts of interest: None reported.
Address correspondence to: Craig G. Crandall, PhD, Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Avenue, Dallas, TX, 75231. E-mail: firstname.lastname@example.org