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目的：观察一氧化氮（ Ｎｉｔｒｉｃ ｏｘｉｄｅ， Ｎ Ｏ）在鞘内注射促肾上腺皮质激素（ Ａｄｒｅｎｏｃｏｒｔｉｃｏｔｒｏｐｉｃｈｏｒｍ ｏｎｅ， Ａ Ｃ Ｔ Ｈ）抑制甲醛大鼠痛敏中的作用。方法：采用脊髓组织 Ｎ Ａ Ｄ Ｐ Ｈｄ 组化染色、原癌基因ｃｆｏｓ 蛋白（ Ｆｏｓ）免疫组化染色及γ氨基丁酸含量测定。结果：鞘内注射 Ａ Ｃ Ｔ Ｈ 显著抑制甲醛痛敏大鼠脊髓内一氧化氮合成酶阳性神经元、 Ｆｏｓ阳性神经元的增多，并提高脊髓内γ氨基丁酸神经递质的含量，且上述作用均为 Ｎ Ｏ前体左旋精氨酸部分逆转。结论：在鞘内注射 Ａ Ｃ Ｔ Ｈ 抑制甲醛大鼠痛敏中， Ｎ Ｏ 合成抑制可能是其重要的分子机制。
Objective: To observe the effect of nitric oxide (N O) on the hyperalgesia of formaldehyde-exposed rats induced by intrathecal Adrenocorticotropichorm one (A C T H). METHODS: The spinal cord tissue was stained with NADP H-d and the proto-oncogene c-fos protein (Fos) immunohistochemical staining and γ-aminobutyric acid content were determined. RESULTS: Intrathecal injection of A C T H significantly inhibited the increase of nitric oxide synthase (NOS) positive neurons and Fos-positive neurons in the spinal cord of formaldehyde-induced hyperalgesia rats, and increased the content of γ-aminobutyric acid neurotransmitter in the spinal cord The above effects are partially reversed by L-arginine, a precursor of NO. CONCLUSION: Inhibition of N O synthesis may be an important molecular mechanism in intrathecal injection of A C T H to inhibit hyperalgesia in rats.