To study the involvement of local sensory nerves in
reactive hyperemia,
laser-Doppler measurements of skin blood flow were recorded in locally anesthetized and untreated forearm sites in eight volunteers after 90, 180, and 360 seconds of arrested forearm blood flow. The
reactive hyperemia increased in magnitude and duration in response to increasing occlusion periods. However, maximum postocclusion flows in the untreated site of 31 +/- 5%, 38 +/- 6%, and 49 +/- 5% (mean +/- SEM) flux were significantly greater than the 14 +/- 3% (P < .005), 20 +/- 4% (P < .005), and 25 +/- 5% (P < .001) flux seen in the anesthetized sites. The duration of the
hyperemia was also shortened from 139 +/- 26 seconds in the untreated site to 61 +/- 17 seconds (after the 360-second occlusion, P < .02) in the anesthetized sites. The
anesthesia did not alter the increase in local blood flow induced by intradermally injected
calcitonin gene-related peptide. Topically applied
capsaicin induced a localized increase in blood flow that was unaffected by
anesthesia and a surrounding flare that was abolished by the treatment. The results show that
local anesthesia can significantly inhibit
reactive hyperemia by a mechanism that does not alter the vasodilation induced by exogenous
calcitonin gene-related peptide or the localized
capsaicin-induced release of
vasodilators from sensory nerves.
Indomethacin was also found to be effective in suppressing
reactive hyperemia. The evidence suggests that postocclusion
reactive hyperemia in human forearm skin is mediated by a local reflex involving sensory nerves and a
cyclooxygenase product, probably a
vasodilator prostaglandin.