Regional relation between skin blood flow and sweating to passive heating and local administration of acetylcholine in young, healthy humans

Smith CJ, Kenney WL, Alexander LM. Regional relation between skin blood flow and sweating to passive heating and local administration of acetylcholine in young, healthy humans. Am J Physiol Regul Integr Comp Physiol 304: R566-R573, 2013. First published February 6, 2013; doi:10.1152/ajpregu.00514.2012.-Regional variation in sweating over the human body is widely recognized yet variation in vasomotor responses and mechanisms causing this variation remain unclear. This study aimed to explore the relation between regional sweating rates (RSR) and skin blood flow (SkBF) responses to thermal and pharmacological stimuli in young, healthy subjects. In nine subjects (23 +/- 3 yr), intradermal microdialysis (MD) probes were inserted into the ventral forearm, abdomen, thigh, and lower back and perfused with lactated Ringer solution. RSR over each MD membrane were measured using ventilated capsules with a laser Doppler probe housed in each capsule for measurement of red cell flux (laser Doppler flux, LDF) as an index of SkBF. Subjects completed a whole body heating protocol to 1 degrees C rise in oral temperature and an acetylcholine dose response (ACh 1 x 10(-7)-0.1 M; mean skin temperature 34 degrees C). Maximal LDF were obtained at the end of both protocols (50 mM sodium nitroprusside). During heating RSR varied among sites (P < 0.0001) and was greater on the back versus other sites (P < 0.05), but LDF was similar between sites (P = 0.343). RSR and SkBF showed a strong relation during initial (arm: r = 0.77 +/- 0.09, thigh: r = 0.81 +/- 0.08, abdomen: r = 0.89 +/- 0.04, back: r = 0.86 +/- 0.04) but not latter stages of heating. No differences in RSR (P = 0.160) or SkBF (LDF, P = 0.841) were observed between sites during ACh perfusion. Taken together, these data suggest that increases in SkBF are necessary to initiate and increase sweating, but further rises in RSR are not fully dependent on SkBF in a doseresponse manner. Furthermore, RSR cannot be explained by cholinergic sensitivity or variation in SkBF.