Evidence for sensory nerve involvement in cutaneous reactive hyperemia in humans.

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.