笑気鎮痛における脊髄グルタメート濃度の変動
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概要
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The mechanism of the hyperalgesia may be mediated by the modulation of the transmission to the WDR neurone from C-fiber in posterior horn of spinal cord. The glutamate in celebrospiral fluid (CSF) are possibly concerned in pain modulation. However, role of these synaptic regulation exerted by concurrent glutamate release and pain response is not fully understood. The purpose of the present study was to investigate whether the inhalation of nitrous oxide modulated pain-related response in relation to glutamate in (CSF) following formalin induced nociception in rats. Three days after intrathecal implantation of PE-10 catheter along with loop-type microdialysis probe in male wister rats, 50μl of 5% formalin was subcutaneously injected into left hind paw. Thereafter, simultaneous determinations of microdialysis at 10 min. -intervals for glutamate by HPLC-THI and observation of flinches were performed for 60 min after inhalation of four type nitrous oxide concentration (control group : 70% nitrogen with 30% oxygen, 30% N2O group : 30% nitrous oxide with 70% oxygen, 50% N2O group : 50% nitrous oxide with 50% oxygen, 70% N2O group : 70% nitrous oxide with 30%). Biphasic increases of flinches after injection of formalin were observed ; phase 1 (13 flinches/min. at 10 min.) and phase 2 (11 flinches/min. at 40 min.). 30% and 50% nitrous oxide attenuated flinches during phase 2 period. 70% nitrous oxide attenuated flinches during both phase 1 and phase 2 periods. CSF glutamate in control group was transiently increased by 145±8% and 126±7% during 10 min and 20 min, respectively. This increase of glutamate was supressed by 30%, 50% and 70% nitrous oxide. The present results clearly demonstrated that nitrous oxide inhibits the both phases of flinchings associated with supressed glutamate release. The analsic effects of nitrous oxide are dose dependence, and these effects may regulate neurotransmitter release evoked by C fiber activation.
- 九州歯科学会の論文
- 2001-04-25