Mert Tufan, Gunes Yasemin, Gunay Ismail
Department of Biophysics, School of Medicine, University of Cukurova, 01330 Balcali, Adana, Turkey.
Eur J Pharmacol. 2007 Oct 31;572(2-3):138-41. doi: 10.1016/j.ejphar.2007.06.026. Epub 2007 Jun 29.
Previous studies has report the modulation of K+ channels play key roles in the induction of peripheral antinociception induced by many types of drugs. However, the possible participation of 4-aminopyridine-sensitive K+ channels to local antinociception induced by tramadol, a mu opioid receptor agonist, and lidocaine, a local anaesthetic, has been less studied. In this study, we therefore investigated this by using thermal plantar test. Tramadol or lidocaine administered intraplantarly into the hind paw elicited an antinociceptive effect. 4-aminopyridine caused an increase in the antinociception produced by lidocaine. However, tramadol induced antinociception remained unaffected by intraplantar administration of 4-aminopyridine. These results suggest that 4-aminopyridine-sensitive K+ channels may play an important role in the thermal peripheral antinociception produced by lidocaine, but not tramadol.
以往的研究报道，钾通道的调节在多种药物诱导的外周抗伤害感受中起关键作用。然而，4-氨基吡啶敏感的钾通道在μ阿片受体激动剂曲马多和局部麻醉药利多卡因诱导的局部抗伤害感受中可能发挥的作用，研究较少。因此，在本研究中，我们通过热足底试验对此进行了研究。将曲马多或利多卡因经足底注射到后爪可产生抗伤害感受作用。4-氨基吡啶可增强利多卡因产生的抗伤害感受作用。然而，曲马多诱导的抗伤害感受不受经足底注射4-氨基吡啶的影响。这些结果表明，4-氨基吡啶敏感的钾通道可能在利多卡因产生的热外周抗伤害感受中起重要作用，但在曲马多产生的热外周抗伤害感受中不起作用。
