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1 Department of Exercise and Movement Science, University of Oregon, Eugene, Oregon 97403-1240; and 2 Department of Anesthesiology, Mayo Clinic and Foundation, Rochester, Minnesota 55905
The mechanisms underlying the skin blood flow
(SkBF) response to local heating are complex and poorly understood. Our
goal was to examine the role of axon reflexes and nitric oxide (NO) in
the SkBF response to a local heating protocol. We performed 40 experiments following a standardized heating protocol with different
interventions, including blockade of the axon reflex (EMLA cream),
antebrachial nerve blockade (0.5% bupivacaine injection), and NO
synthase (NOS) inhibition (
10 mM
NG-nitro-L-arginine methyl
ester; microdialysis). Appropriate controls were performed to verify
the efficacy of the various blocks. Values are expressed as a
percentage of maximal SkBF (SkBFmax; 50 mM sodium
nitroprusside). At the initiation of local heating, SkBF rose
to an initial peak, followed by a brief nadir, and a secondary, progressive rise to a plateau. Axon reflex block decreased the initial
peak from 75+3 to 32 ± 2% SkBFmax (P < 0.01 vs. control) but did not affect the plateau. NOS inhibition
before and throughout local heating reduced the initial peak from
75 ± 3 to 56 ± 3% SkBFmax (P < 0.01) and the plateau from 87 ± 4 to 40 ± 5%. NOS inhibition during axon reflex block did not further reduce the initial
SkBF peak compared with axon reflex block alone. Antebrachial nerve
block did not affect the local heating SkBF response. The primary
finding of these studies is that there are at least two independent
mechanisms contributing to the rise in SkBF during nonpainful local
heating: a fast-responding vasodilator system mediated by the axon
reflexes and a more slowly responding vasodilator system that relies on
local production of NO.
cutaneous vascular conductance; axon reflex; human; microvascular dysfunction
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