Nitric oxide in hyperbaric oxygen-induced acute antinociception in mice
Nitric oxide in hyperbaric oxygen-induced acute antinociception in mice
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DOI：
10.1097/wnr.0b013e3283305a49
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发表时间：
2009-10-07
期刊：
影响因子：
1.7
通讯作者：
Quock, Raymond M.
中科院分区：
文献类型：
--
作者：
Ohgami, Yusuke;Zylstra, Carlyn C.;Quock, Raymond M.
高压氧（HBO 2）疗法在人类的各种疼痛条件下诱导镇痛。在小鼠中，HBO 2治疗在腹部收缩试验中引起急性抗伤害性反应。为了证明HBO 2诱导的抗伤害感受对一氧化氮（NO）的依赖性，在三种不同的干扰NO产生的方法后评估对HBO 2的抗伤害感受反应。HBO 2诱导的抗伤害作用显着衰减脑室内和鞘内预处理与一氧化氮合酶（NOS）酶的抑制剂，也通过针对神经元NOS的反义寡脱氧核苷酸。在神经元NOS基因缺陷的纯合子小鼠中，抗伤害效应也显著降低。在这些结果的基础上，我们得出结论，神经元NO的表达是至关重要的急性抗伤害效应的HBO 2。NeuroReport 20：1325-1329（C）2009年威科健康垂直酒吧Lippincott威廉姆斯&威尔金斯。
Hyperbaric oxygen (HBO2) therapy induces analgesia in various conditions of pain in humans. In mice, HBO2 treatment evokes an acute antinociceptive response in the abdominal constriction test. To demonstrate the dependence of HBO2-induced antinociception on nitric oxide (NO), antinociceptive responsiveness to HBO2 was assessed after three different approaches that interfered with NO production. HBO2-induced antinociception was significantly attenuated by intracerebroventricular and intrathecal pretreatment with an inhibitor of NO synthase (NOS) enzyme and also by an antisense oligodeoxynucleotide directed against neuronal NOS. The antinociceptive effect was also significantly reduced in mice homozygous for a defective neuronal NOS gene. On the basis of these results, we conclude that neuronal NO is critical in the expression of the acute antinociceptive effect of HBO2. NeuroReport 20:1325-1329 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.