• S Kalman, C Linderfalk, K Wårdell, C Eintrei, and B Lisander.
• Department of Anesthesiology, University Hospital, Linköping, Sweden. Sigga.Kalman@ane.us.lio.se
• Reg Anesth Pain Med. 1998 Jul 1;23(4):402-8.

Background And ObjectivesWhen given intracutaneously, capsaicin can cause burning pain by central propagation in thin afferents, as well as neurogenic vasodilatation, reflecting antidromic conduction in the same fibers. We wanted to test the hypothesis that an intravenous regional block (IVRA) inhibits these two phenomena to a similar degree.MethodsSixteen healthy volunteers participated. A bilateral IVRA was performed by simultaneously injecting mepivacaine in one arm and normal saline in the other in a randomized, double-blind manner. Ten minutes after release of the tourniquet, neurogenic inflammation was inflicted in each forearm by intracutaneous capsaicin. Microvascular skin blood flow was measured with a laser Doppler perfusion imager. The area of the flare and the flow therein were measured, taking into account the change in baseline caused by mepivacaine treatment and the postischemic hyperemia. Pain was repeatedly evaluated by visual analog scale.ResultsThe reactive hyperemia following arterial occlusion was less in the mepivacaine-treated arm 10 minutes after tourniquet release (P=.026). Intracutaneous capsaicin elicited a flare in both arms. The area of the flare was smaller 10 minutes after capsaicin (P=.009) in the mepivacaine-treated arm. There was no difference between the arms concerning the mean blood flow within the flare or in ischemic or capsaicin-induced pain.ConclusionsMepivacaine, given as an IVRA, had no effect on the post-IVRA sensory function of thin afferents but differentially decreased the spread of the capsaicin-induced flare.

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