Muscle pain is quite common, but its mechanism is not well understood. For analyzing peripheral mechanism of muscle pain, importance of non-invasive method evaluating pressure pain threshold (mechanical withdrawal threshold in animals) was discussed. For experimental model analyzing muscle pain mechanism, delayed onset muscle soreness model was developed by applying lengthening contraction (LC) to rats, and results obtained in this model was introduced. Existence of mechanical hyperalgesia in this model was demonstrated by measuring mechanical withdrawal threshold by Randall-Selitto apparatus equipped with a large probe with tip diameter of 2.6 mm and by examining c-Fos expression in the superficial dorsal horn. Increase in mechanical sensitivity (decrease in threshold and increase in response magnitude) of muscle C-fiber nociceptors was demonstrated by single nerve recording in vitro in the muscle which were hyperalgesic 2 days after LC, and this change is considered to be the peripheral mechanism for mechanical hyperalgesia after exercise. Absence of muscle damage and inflammation, existence of taut band and referred pain by compressing the taut band in this model suggest that this model will be suitable and useful for the study of neural mechanism of clinically important muscle pain conditions.

抄録全体を表示

   Although opioids are known to have a local analgesic action by nerve conduction block, it remains to be unclear whether this action is due to opioid-receptor activation. We have previously reported that a non-narcotic opioid tramadol more effectively inhibits compound action potentials (CAPs) than its metabolite mono-O-demethyl-tramadol (M1) in a manner independent of opioid-receptor activation and that this difference in inhibition between the two opioids may be due to a distinction between their chemical structures. To address further this issue, we examined the effects of opioids (morphine, codeine, ethylmorphine and dihydrocodeine) and cocaine on CAPs by applying the air-gap method to frog sciatic nerves. All of the opioids at concentrations less than 10 mM reduced the peak amplitude of the CAP in a reversible and dose-dependent manner; this action was resistant to a nonspecific opioid-receptor antagonist naloxone. The sequence of the CAP peak amplitude reductions was ethylmorphine (IC₅₀ = 4.6 mM) > codeine > dihydrocodeine ≥ morphine; this opioid-mediated inhibition was much less than that of cocaine (IC₅₀ = 0.80 mM). The CAP peak amplitude reductions produced by morphine, codeine and ethylmorphine were related to their chemical structures in such that this extent enhanced with an increase in the number of -CH₂ in a benzene ring, as seen in the inhibitory actions of tramadol and M1. It is suggested that the substituted groups of -OH bound to the benzene ring of morphine, codeine and ethylmorphine as well as tramadol and M1 may play an important role in producing nerve conduction block.

抄録全体を表示