BACKGROUND AND OBJECTIVES: In previous studies we have demonstrated that after intravenous regional block (IVRA) with dilute mepivacaine, there is a decrease in neurogenic inflammation as well as in post-ischemic hyperemia and steady-state flow, the latter for at least 60 minutes. It is unclear whether these vascular reactions reflect a uniform depression of nerve function in the treated arms. Because the various afferents convey impulses from different types of sensory receptors, we used quantitative sensory testing (QST) to define these effects of IVRA with mepivacaine. METHODS: In 16 volunteers, bilateral blocks were performed by simultaneously injecting mepivacaine in one arm and normal saline in the other in a randomized, double-blind manner. Both arms were kept ischemic for 20 minutes, and the pain was rated on a visual analogue scale. Skin temperature and perception threshold values regarding touch (Abeta-fibers), warmth (C-fibers) and cold (Adelta-fibers), and heat pain (C-fibers) were determined before and repeatedly after the blocks. RESULTS:Ischemic pain did not differ between the arms. After reflow, the thresholds for touch, warmth, and heat pain were unchanged. In the mepivacaine-treated arm, the sensibility to cold was significantly decreased 10 and 30 minutes after the block, though there was a slight decrease in skin temperature. CONCLUSIONS: There was no uniform depression of nerve function after IVRA. The cold receptors and/or their Adelta-fibers were selectively depressed after the block. In conjunction with earlier findings, this suggests that IVRA with mepivacaine can differentially decrease neurogenic inflammation, with little impairment of sensory function.
RCT Entities:
BACKGROUND AND OBJECTIVES: In previous studies we have demonstrated that after intravenous regional block (IVRA) with dilute mepivacaine, there is a decrease in neurogenic inflammation as well as in post-ischemic hyperemia and steady-state flow, the latter for at least 60 minutes. It is unclear whether these vascular reactions reflect a uniform depression of nerve function in the treated arms. Because the various afferents convey impulses from different types of sensory receptors, we used quantitative sensory testing (QST) to define these effects of IVRA with mepivacaine. METHODS: In 16 volunteers, bilateral blocks were performed by simultaneously injecting mepivacaine in one arm and normal saline in the other in a randomized, double-blind manner. Both arms were kept ischemic for 20 minutes, and the pain was rated on a visual analogue scale. Skin temperature and perception threshold values regarding touch (Abeta-fibers), warmth (C-fibers) and cold (Adelta-fibers), and heat pain (C-fibers) were determined before and repeatedly after the blocks. RESULTS: Ischemic pain did not differ between the arms. After reflow, the thresholds for touch, warmth, and heat pain were unchanged. In the mepivacaine-treated arm, the sensibility to cold was significantly decreased 10 and 30 minutes after the block, though there was a slight decrease in skin temperature. CONCLUSIONS: There was no uniform depression of nerve function after IVRA. The cold receptors and/or their Adelta-fibers were selectively depressed after the block. In conjunction with earlier findings, this suggests that IVRA with mepivacaine can differentially decrease neurogenic inflammation, with little impairment of sensory function.