THE SYMPATHETIC NERVOUS-SYSTEM CONTRIBUTES TO CAPSAICIN-EVOKED MECHANICAL ALLODYNIA BUT NOT PINPRICK HYPERALGESIA IN HUMANS

The contribution of the sympathetic nervous system (SNS) to pain, mech anical allodynia (MA), and hyperalgesia in humans is controversial. A clearer understanding is crucial to guide therapeutic use of sympathol ytic surgery, blocks, and drug treatments. In rats, capsaicin-evoked M A, and to some extent, pinprick hyperalgesia (PPH), can be blocked wit h alpha-adrenoreceptor antagonists. In this study, we examined the con tribution of the SNS to MA and PPH in normal human subjects by blockin g alpha-adrenoreceptors with intravenous phentolamine. In a double-bli nded, placebo-controlled, crossover study, subjects were given IV sali ne or phentolamine, 1 mg/kg over 20 min. Ten minutes after the start o f the infusion, subjects received 100 mu g of intradermal capsaicin on the foot dorsum with the temperature of the injected site clamped at 36 degrees C. The temperature of the uninjected foot was used to monit or the degree of cv-adrenoreceptor blockade produced by phentolamine. Ongoing pain and MA and PPH areas were measured every 5 min for 60 min . A significantly greater increase in temperature on the uninjected fo ot was seen during the phentolamine infusion compared with the saline infusion, indicating alpha-adrenergic blockade. Significantly less MA was observed with the phentolamine infusion 10-25 min after capsaicin injection than with the saline infusion. No significant differences in ongoing pain or PPH areas were seen between the two infusions at any time. Our results suggest that capsaicin-evoked MA and PPH have differ ent mechanisms, with the SNS having a role in MA but not in PPH or ong oing pain.