Abstract
Local anesthetic efficacy of tramadol has been reported following intradermal application. Our aim was to investigate the effect of perineural tramadol as the sole analgesic in two pain models. Male Wistar rats (280-380 g; N = 5/group) were used in these experiments. A neurostimulation-guided sciatic nerve block was performed and 2% lidocaine or tramadol (1.25 and 5 mg) was perineurally injected in two different animal pain models. In the flinching behavior test, the number of flinches was evaluated and in the plantar incision model, mechanical and heat thresholds were measured. Motor effects of lidocaine and tramadol were quantified and a motor block score elaborated. Tramadol, 1.25 mg, completely blocked the first and reduced the second phase of the flinching behavior test. In the plantar incision model, tramadol (1.25 mg) increased both paw withdrawal latency in response to radiant heat (8.3 ± 1.1, 12.7 ± 1.8, 8.4 ± 0.8, and 11.1 ± 3.3 s) and mechanical threshold in response to von Frey filaments (459 ± 82.8, 447.5 ± 91.7, 320.1 ± 120, 126.43 ± 92.8 mN) at 5, 15, 30, and 60 min, respectively. Sham block or contralateral sciatic nerve block did not differ from perineural saline injection throughout the study in either model. The effect of tramadol was not antagonized by intraperitoneal naloxone. High dose tramadol (5 mg) blocked motor function as well as 2% lidocaine. In conclusion, tramadol blocks nociception and motor function in vivo similar to local anesthetics.
Highlights
Tramadol, (1-RS,2RS)-2-[(dimethyl-amino)-methyl]1-(3-methoxyphenyl)-cyclohexanol hydrochloride, is a centrally acting analgesic commercialized as a racemic mixture of two enantiomers [(+) and (-) tramadol]
Sciatic nerve block Perineural injection of 2% lidocaine completely blocked motor function in the hind paw of all rats, which was recovered over time in a gradual way that allowed the construction of a motor block score (Table 1)
We demonstrated that tramadol blocked nerve conduction in rats similar to lidocaine
Summary
Tramadol, (1-RS,2RS)-2-[(dimethyl-amino)-methyl]1-(3-methoxyphenyl)-cyclohexanol hydrochloride, is a centrally acting analgesic commercialized as a racemic mixture of two enantiomers [(+) and (-) tramadol]. In addition to its central analgesic effects, tramadol exhibits a local anesthetic effect following intradermal injection and acts as a sole anesthetic in tendon repair surgery [4,5]. Consistent with these findings, tramadol, but not its metabolite M1, blocks voltage-dependent sodium channels and suppresses somatosensory potentials following intrathecal administration through a mechanism not involving opioid receptors [6,7,8]. Tramadol decreases sensory and motor responses evoked by electroneurography of the ulnar nerve in volunteers [9] and acts as an adjuvant after intra-articular injection [10] and peripheral nerve blocks, prolonging sensory and motor effects [11]
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