A prolonged nitric oxide-dependent, opioid-mediated antinociceptive effect of hyperbaric oxygen in mice.
A prolonged nitric oxide-dependent, opioid-mediated antinociceptive effect of hyperbaric oxygen in mice.
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DOI：
10.1016/j.jpain.2008.08.003
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发表时间：
2009-02
期刊：
影响因子：
--
通讯作者：
Quock RM
中科院分区：
文献类型：
--
作者：
Zelinski LM;Ohgami Y;Chung E;Shirachi DY;Quock RM
据报道，高压氧（HBO2）治疗可以缓解几种慢性疼痛。单次60分钟的HBO2治疗在小鼠中产生了持续90分钟的抗伤害感受作用。在HBO2暴露前，阿片拮抗剂纳曲酮、非特异性一氧化氮合酶抑制剂ng -硝基- l-精氨酸甲酯（L-NAME）和选择性神经元一氧化氮合酶抑制剂s -甲基- l-硫氨酸（SMTC）可以显著减弱HBO2诱导的抗痛感，但选择性内皮一氧化氮合酶抑制剂N5-（1-亚氨基乙基）- l-鸟氨酸（L-NIO）不能减弱HBO2诱导的抗痛感。兔dynorphin1-13抗血清中央预处理也能显著降低抗痛觉作用，而兔β-内啡肽或蛋氨酸-脑啡肽抗血清无明显作用。在HBO2诱导治疗90分钟后，纳曲酮显著减弱了抗伤害性效果，但在HBO2治疗60分钟后，在伤害性测试之前给予L-NAME则没有。这些发现表明，HBO2暴露后持续90分钟的抗痛觉作用是由一氧化氮（NO）和阿片机制介导的，但一氧化氮的参与在HBO2治疗期间至关重要，而不是在伤害性测试时。这些结果与HBO2可能诱导no依赖性阿片肽释放从而产生长效抗伤害感受作用的概念一致。
Hyperbaric oxygen (HBO2) therapy is reported to cause pain relief in several conditions of chronic pain. A single 60-min session of HBO2 treatment produced a prolonged antinociceptive effect in mice that persisted for 90 min after cessation of treatment. The HBO2-induced antinociception was significantly attenuated by pretreatment prior to HBO2 exposure with the opioid antagonist naltrexone, the non-specific nitric oxide synthase (NOS)-inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and the selective neuronal NOS-inhibitor S-methyl-L-thiocitrulline (SMTC) but not the selective endothelial NOS-inhibitor N5-(1-iminoethyl)-L-ornithine (L-NIO). The antinociception was also significantly reduced by central pretreatment with a rabbit antiserum against dynorphin1-13 but not by rabbit antisera against either β-endorphin or methionine-enkephalin. The prolonged antinociceptive effect at 90 min after HBO2-induced treatment was also significantly attenuated by naltrexone but not L-NAME administered 60 min following HBO2 treatment but prior to nociceptive testing. These findings indicate that the antinociception that persists for 90 min after HBO2 exposure is mediated by nitric oxide (NO) and opioid mechanisms but that the NO involvement is critical during the HBO2 treatment and not at the time of nociceptive testing. These results are consistent with the concept that HBO2 may induce an NO-dependent release of opioid peptide to cause a long-acting antinociceptive effect.
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