尾核内一氧化氮对大鼠痛行为的影响

Effects of Nitric Oxide on Pain Threshold in Rat Caudate Nucleus

目的观察大鼠尾核内一氧化氮、一氧化氮合酶抑制剂和鸟苷酸环化酶抑制剂对动物痛阈(痛行为)的影响。方法以钾离子透入引起大鼠甩尾的电流强度(mA)作为痛反应指标,尾核内微量注射L-精氨酸、Nω-硝基-L-精氨酸甲酯、亚甲基蓝等,观察0～30min内大鼠痛阈的变化。结果大鼠尾核内微量注射一氧化氮的前体Nω-硝基-L-精氨酸甲酯引起明显的痛敏效应,20min内与对照组比较有显著性差异(P<0.05)。微量注射Nω-硝基-L-精氨酸甲酯和亚甲基蓝后大鼠痛阈显著升高,25min内与对照组比较有显著性差异(P<0.05)。结论提示中枢神经系统内一氧化氮具有明显的痛敏效应,而降低中枢神经系统一氧化氮水平表现显著的镇痛作用。其作用机理可能和NO-cGMP代谢途径有关。

Objective To observe the effects of nitric oxide （NO）,inhibitors of nitric oxide synthase and guanylate cyclase on pain threshold of rats. Methods Pain threshold （PT） determined by measurements of potassium iontophoresis induced - tail - flick, PT changes were observed after micro - injection of L - arginine （L - Arg）, N （omega） - nitro - L- arginine methylester （L - NAME） and methylene blue （MB） into rat caudate nucleus within 30 minutes, Results Compared with the control group,significant hyperalgesic effects were observed after micro- injection of L - Arg into rat caudate nucleus/There were statistical significance within 20 minutes （P〈 0,05）, PT of rats was increased significantly after micro- injection of L- NAME and MB, There were statistical significance in the treatment groups within 25 minutes compared with control group （P 〈 0.05）. Conclusion Increased NO level in central nervous system （CNS） produced hypoalgesia and decreased NO level produced analgesia,The effects of NO on modulation of CNS pain in rats may be partially mediated by NO - cGMP metabolic pathway,