Effect of tramadol on behavioral alterations and lipid peroxidation after transient forebrain ischemia in rats

• Published in: Toxicology mechanisms and methods Vol. 22; no. 9; pp. 674 - 678
• Main Authors: Nagakannan, Pandian, Shivasharan, Basavaraj D., Thippeswamy, Boreddy S., Veerapur, Veeresh P.
• Format: Journal Article
• Language: English
• Published: England Informa Healthcare 01.11.2012; Taylor & Francis
• Subjects: Animals; Behavior, Animal - drug effects; Dose-Response Relationship, Drug; forebrain ischemia; Ischemic Attack, Transient - complications; Ischemic Attack, Transient - drug therapy; Ischemic Attack, Transient - metabolism; Ischemic Attack, Transient - physiopathology; Lipid Peroxidation - drug effects; Male; Malondialdehyde - metabolism; Motor Activity - drug effects; neuroprotective; Neuroprotective Agents - administration & dosage; Neuroprotective Agents - therapeutic use; NMDA antagonist; opioid agonist; Prosencephalon - blood supply; Prosencephalon - drug effects; Prosencephalon - metabolism; Rats; Rats, Wistar; Reperfusion Injury - etiology; Reperfusion Injury - metabolism; Reperfusion Injury - physiopathology; Reperfusion Injury - prevention & control; sensorimotor function; Tramadol; Tramadol - administration & dosage; Tramadol - therapeutic use
• ISSN: 1537-6516; 1537-6524
• DOI: 10.3109/15376516.2012.716092

N-methyl-D-aspartate (NMDA) antagonists and γ-aminobutyric acid (GABA) agonists are proven protective in various animal models of ischemic brain damage. Tramadol, a centrally acting opioid analgesic reportedly possesses NMDA antagonistic and GABA agonistic properties, with additional ion channel blocking activity. The aim of the present study was to evaluate the possible neuroprotective effect of tramadol hydrochloride in a rat model of transient forebrain ischemia. Male Wistar rats were pretreated with tramadol hydrochloride at doses of 10 and 20 mg/kg b.w. intraperitoneally for 4 days and were subjected to 30 min occlusion of bilateral common carotid arteries followed by reperfusion for 24 h. Impairment in sensorimotor functions was evaluated by beam walking task, spontaneous locomotor activity and hanging wire test. Animals were sacrificed and the brain homogenates were used for estimating the levels of lipid peroxidation, a marker for extent of oxidative stress. Ischemic rats exhibited a significant decrease in locomotion, grip strength and increase in beam walking latency. Tramadol attenuated the post ischemic motor impairment evidenced by improvement in the performance in sensorimotor tests. The extent of lipid peroxidation was significantly (p < 0.001) reduced by tramadol pretreatment which was higher in ischemic control. This study demonstrates the neuroprotective effect of tramadol against transient forebrain ischemia in rats.