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Effects of dexmedetomidine on conditioned pain modulation in humans
Author(s) -
Baba Y.,
Kohase H.,
Oono Y.,
FujiiAbe K.,
ArendtNielsen L.
Publication year - 2012
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1002/j.1532-2149.2012.00129.x
Subject(s) - dexmedetomidine , agonist , diffuse noxious inhibitory control , stimulation , saline , anesthesia , medicine , conditioning , systemic administration , pharmacology , noxious stimulus , nociception , receptor , sedation , biology , in vivo , statistics , mathematics , microbiology and biotechnology
Background Systemic administration of dexmedetomidine ( DEX ; selective α 2 ‐adrenoceptor agonist) is found to inhibit diffuse noxious inhibitory control in rats, now referred to as conditioned pain modulation ( CPM ) in humans. The present study was designed to investigate the effect of intravenous administration of DEX on CPM in humans. Methods There were two sequential sessions in this double blind, randomized study. The first session was the control with normal saline infusion ( N 1st , L 1st , H 1st ). During the second session, three types of agents were infused: normal saline ( N 2nd ); a low plasma concentration of DEX (0.04 ng/mL; L 2nd ); and a high plasma concentration of DEX (0.08 ng/mL; H 2nd ). The amplitude of somatosensory evoked potentials (amp SEP )s and the visual analogue scale of tooth pain ( VASt ) induced by electrical tooth stimulation were evaluated with and without conditioning CO 2 laser stimulation of the hand. The inhibition rate (% inhibition) was calculated [= (1‐[amp SEP or VASt with conditioning stimuli]/[amp SEP or VASt without conditioning stimuli]) × 100] to compare the magnitude of the DEX effects on CPM . Results The inhibition rates of amp SEP s and VASt in Types N , L and H varied significantly, demonstrating a dose‐dependent reduction of CPM effects of amp SEP and VASt during randomized DEX administration, consistent with results from animal studies. Conclusions The present study shows that systemic administration of an α 2 ‐adrenoceptor agonist ( DEX ), less than the clinical dose, inhibited CPM in humans. These results may provide some mechanistic insight into why many chronic pain patients show impaired CPM .