抄録
Although tramadol is known to exhibit a local anesthetic effect following intradermal injection, this action has not been examined yet thoroughly. The present study examined the effects of tramadol and its metabolite mono-O-demethyl-tramadol (M1) on compound action potentials (CAPs) by applying the air-gap method to frog sciatic nerves; these results were compared with those of well-known local anesthetics, lidocaine and ropivacaine. Tramadol dose-dependently reduced the peak amplitude of the CAP (IC50 = 2.3 mM). On the other hand, M1, which exhibits a higher affinity for μ-opioid receptors than tramadol does, at concentrations less than 2 mM did not affect CAPs, albeit the peak amplitude was reduced at 5 mM by 9%. Such an effect of tramadol was resistant to a nonspecific opioid-receptor antagonist naloxone (10 μM); a μ-opioid receptor agonist DAMGO (1 μM) did not affect CAPs. The CAP peak amplitude reduction produced by tramadol was less in extent than those of lidocaine and ropivacaine (IC50: 0.74 mM and 0.34 mM, respectively), and the former action was slower in recovery than the latter two ones. These results indicate that tramadol reduces CAP peak amplitudes in peripheral nerve fibers in a manner independent of μ-opioid receptors with a potency which is less than those of lidocaine and ropivacaine, and with a slower time course compared to them, whereas M1 has much less effect on CAPs. The methyl group present in tramadol but not M1 is suggested to play an important role in producing nerve conduction block. [J Physiol Sci. 2007;57 Suppl:S226]
