Abstract
The Background: Tramadol, is a central acting analgesic that possesses weak affinity for the μ-opioid receptor and modifies transmission of nociceptive impulses through inhibition of monoamine reuptake. This study was designed to determine the effect of tramadol on blood glucose levels and also to investigate whether or not alpha-2 adrenergic receptors were responsible for this effect. Methods: Twenty-five Wistar male rats were assigned to four groups to receive: Group I: saline; Group II: tramadol (1 mg·kg-1); Group III and Group IV: pretreatment with a2-receptor antagonist drugs yohimbine (1 mg·kg-1) or idazoxan (1 mg·kg-1), 30 min before administration of tramadol (1 mg·kg-1). Samples for plasma glucose measurement were withdrawn at 0, 30, 60, 90 and 120 minutes of the experiment. Results: A significant rise in blood glucose levels was observed following administration of i.v. tramadol. Pretreatment with both yohimbine and idazoxan (1 mg·kg-1) significantly attenuated tramadol-induced hyperglycemia. Conclusion: The results of the study indicate that, tramadol administered at an analgesic dose of 1 mg·kg-1 produces hyperglycemia in diethyl ether anesthetized rats. Reversal of this effect with a2-adrenoceptor blocking agents suggests that monoaminergic pathways which contribute to the analgesic action of tramadol, may have a role in the hyperglycemic action of the drug.
Highlights
The central acting, synthetic analgesic tramadol [tramadol hydrochloride is (±) cis-2-[(dimethylamino) methyl]1-(3-methoxyphenyl) cyclohexanol hydrochloride] has a low affinity for μ-opioid receptors which may not adequately explain its analgesic and antinociceptive potency and its effects are distinct from those of the pure opioid agonists available in clinical practice [1,2,3].Besides the known opioid involvement in modulation of pain, a supraspinal monoaminergic neuronal system that modulates nociceptive processes in the spinal cord has been documented [3]
Normal saline administered to rats in group I did not cause a change in plasma glucose levels compared to basal values
There was no significant difference in plasma glucose levels in rats which were pretreated with idazoxan and the group receiving only saline (102.14 ± 17.77 mg/dL versus 116.75 ± 9.84 mg/dL at 0 min; 111.00 ± 10.39 mg/dL versus 131.50 ± 8.54 at 30 min; 113.00 ± 16.04 mg/dL versus 132.50 ± 6.60 mg/dL at 60 min; 120.29 ± 14.60 mg/dL versus 134.75 ± 14.56 mg/dL at 90 min; and 118.00 ± 13.86 mg/dL versus 134.75 ± 26.39 mg/dL at 120 min). The results of this present study have shown that, tramadol hydrochloride; administered at an antinociceptive dose of 1 mg·kg−1 induce a significant hyperglycemic response in normal fasted rats
Summary
The central acting, synthetic analgesic tramadol [tramadol hydrochloride is (±) cis-2-[(dimethylamino) methyl]1-(3-methoxyphenyl) cyclohexanol hydrochloride] has a low affinity for μ-opioid receptors which may not adequately explain its analgesic and antinociceptive potency and its effects are distinct from those of the pure opioid agonists available in clinical practice [1,2,3].Besides the known opioid involvement in modulation of pain, a supraspinal monoaminergic neuronal system that modulates nociceptive processes in the spinal cord has been documented [3]. The monoaminergic and opioid systems possess receptors and transmitters located on the same cells and, as shown in receptor blocking studies, the synergistic activity of these two systems achieve an antinociceptive effect [2,4,6,7,8]. Both adrenaline a mixed adrenergic agonist and clonidine an 2-adrenergic agonist, induce an increase in blood glucose levels through activation of 2-adrenoceptors. Results of previous studies have shown that 2-adrenoceptor induced hyperglycemia was abolished in animals pretreated with 2-adrenoceptor antagonists [10,12,13]
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