This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Ulger, F. Articles by Güldogus, F. PubMed Articles by Ulger, F. Articles by Güldogus, F. Related Collections Mechanisms Pain Mechanisms Preclinical Pharmacology Pain Pharmacology

---

ANALGESIA

The Antinociceptive Effects of Intravenous Dexmedetomidine in Colorectal Distension-Induced Visceral Pain in Rats: The Role of Opioid Receptors

Fatma Ulger, MD^*, Ayhan Bozkurt, PhD, S. Srr Bilge, MD, Fatih lkaya, MD, Ahmet Dilek, MD^*, M. Ömer Bostanci, PhD, Engin Çiftciolu, MD^||, and Fuat Güldou, MD^*

From the Departments of *Anesthesiology and Reanimation, Physiology, Pharmacology, and ||Anatomy, Ondokuz Mays University, School of Medicine, Samsun, and Hitit University, School of Health, Corum, Turkey.

Address correspondence and reprint requests to Ayhan Bozkurt, PhD, Department of Physiology, Ondokuz Mays University, School of Medicine, Kurupelit, Samsun, Turkey. Address e-mail to abozkurt{at}omu.edu.tr or bozkurtayhan{at}hotmail.com.

Abstract

BACKGROUND: In comparison with cutaneous pain, the role of ₂-adrenoceptor (₂-AR) agonists in visceral pain has not been extensively examined. We aimed to characterize the antinociceptive effect of IV dexmedetomidine on visceral pain in rats and to determine whether antinociception thus produced is mediated by opioid receptors.

METHODS: Male Sprague Dawley rats (250–300 g) were instrumented with a venous catheter for drug administration and with enameled nichrome electrodes for electromyography of the external oblique muscles. Colorectal distension (CRD) was used as the noxious visceral stimulus, and the visceromotor response to CRD was quantified electromyographically before and 5, 15, 30, 60, 90, and 120 min after dexmedetomidine or clonidine administration. Antagonists were administered 10 min before dexmedetomidine. After confirmation of normal distribution of data, one-way analysis of variance with the Tukey-Kramer post hoc test was used for multiple comparison.

RESULTS: IV administration of dexmedetomidine (2.5–20 µg/kg) and clonidine (10–80 µg/kg) produced a dose-dependent reduction in visceromotor response with 50% effective dose values of 10.5 and 37.6 µg/kg, respectively. Administration of the nonspecific ₂-AR antagonist yohimbine (1 mg/kg), but not the peripherally restricted ₂-AR antagonist MK-467 (1 mg/kg), abolished the antinociceptive effect of dexmedetomidine (10 µg/kg). In addition, inhibition of opioid receptors by naloxone (1 mg/kg) attenuated the antinociceptive effect of dexmedetomidine.

CONCLUSION: Our data indicate that IV dexmedetomidine exerts pronounced antinociception against CRD-induced visceral pain and suggest that the antinociceptive effect of dexmedotimidine is mediated in part by opioid receptors, but peripheral ₂-ARs are not involved.