摘要
目的 探讨羟自由基 (·OH)参与疼痛调控的机制。方法 分别用Ca2 + 通道阻滞剂维拉帕米 (Ver)及N 甲基 D 天 (门 )冬氨酸 (NMDA)受体非竞争性拮抗剂氯氨酮 (Ket)预处理观察·OH的中枢致痛敏作用与Ca2 + 、NMDA受体之间的关系 ;并测定小鼠疼痛过程中脊髓、脑、血中前列腺素(PGs)的含量。结果 Ver(5mg/kg ,ip)、Ket(30mg/kg ,ip ;0 5mg/kg ,ith)可拮抗·OH的致痛敏作用 ,但icv·OH后不影响PGs的含量。结论 ·OH的中枢致痛敏作用的机制可能与细胞内高钙及NMDA受体的激活有关。
Objective To study the mechanism of pain modulation effect of ·OH. Methods Calcium channel blocker Ver or N-methyl-D-aspartate (NMDA) receptor noncompetitive antagonist-Ket was pre-administrated to observe the change of hyperalgesia effect induced by ·OH on mice. The concentration of PG was measured 30 min after icv ·OH. Results Ver 5 mg/kg or Ket 30 mg/kg ip, Ket 0.5 mg/kg ith all off-set the hyperalgesia effect of ·OH. But no change in PG concentration was observed. Conclusion The increase of intracellular Ca 2+ concentration and the activation of NMDA-R contribute to the hyperalgesia effect of ·OH.
出处
《安徽医科大学学报》
CAS
2003年第3期168-171,共4页
Acta Universitatis Medicinalis Anhui
基金
安徽省教育厅科研基金资助项目 (编号 :99j10 10 3 )
