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 wa...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 Samples for plasma glucose measurement were withdrawn at 0, 30, 60, 90 and 120 minutes of the experiment.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.展开更多
文摘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 Samples for plasma glucose measurement were withdrawn at 0, 30, 60, 90 and 120 minutes of the experiment.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.
