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PAIN MEDICINE

-1 and -2 Adrenergic Antagonists Relieve Thermal Hyperalgesia in Experimental Mononeuropathy from Chronic Constriction Injury

Department of Anesthesiology, Division of Pain Medicine, Emory University School of Medicine, Atlanta, Georgia

Address correspondence and reprint requests to Allen H. Hord, MD, Department of Anesthesiology, Emory University School of Medicine, 1364 Clifton Rd. N.E., Atlanta, GA 30322. Address e-mail to allen_hord{at}emory.org

Abstract

Phentolamine, a nonspecific 1- and 2-adrenergic antagonist, relieves pain in patients with reflex sympathetic dystrophy. We sought to determine whether phentolamine, prazosin (1 antagonist), or SKF86466 (2 antagonist) relieve thermal hyperalgesia in rats with neuropathic pain. Four days after producing a chronic constriction injury (CCI), thermal hyperalgesia was tested by measuring paw withdrawal latency (PWL). After injection of phentolamine, prazosin, or SKF86466 each at doses of 1, 2, or 5 mg/kg, PWL tests were measured at 5 min and repeated at 15-min intervals for 1 h. Phentolamine, prazosin, and SKF86466 1, 2, and 5 mg/kg provided statistically significant analgesia in rats with CCI for at least 65 min. PWL did not return to baseline levels after 1 or 2 mg/kg of prazosin or SKF86466 but did so after 35 min after phentolamine 2 mg/kg. After 5 mg/kg, PWL returned to preoperative values between 5 and 50 min for phentolamine, at 35 and 65 min for prazosin, and at 50 min for SKF86466. We conclude that both 1 and 2 peripheral receptors of the sympathetic nervous system are involved in the thermal hyperalgesia caused by CCI and that thermal hyperalgesia can be reversed by both 1 and 2 antagonists in a dose-dependent manner.

Implications: Thermal hyperalgesia in the chronic constriction injury model of mononeuropathy is mediated by receptors. Although 1 and mixed 1- and 2-receptor antagonists have been used in humans to treat reflex sympathetic dystrophy, drugs that are highly specific postjunctional 2 antagonists may also be useful in the treatment of sympathetically mediated pain.

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