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本文采用ＮＡＤＰＨｄ组化染色技术，研究鞘内注射（ｉ．ｔ．）ＡＣＴＨ及电针剌激（ＥＡ）对甲醛痛敏大鼠脊髓背角浅层ＮＯＳ阳性神经元增多的影响。结果显示ＡＣＴＨ（０．５Ｕ，ｉ．ｔ．）及电针（１ｍＡ５０Ｈｚ，５ｍＡ５Ｈｚ，１ｍＡ５Ｈｚ）剌激“夹脊穴”３０ｍｉｎ均可显著抑制脊髓背角浅层ＮＯＳ阳性神经元增多；ｉ．ｔ．ＡＣＴＨ（０．５Ｕ）和电针剌激（１ｍＡ５Ｈｚ）同时给予时，抑制作用显著增加；ｉ．ｔ．ＮＯ前体左旋精氨酸（ＬＡｒｇ，１０ｎｍｏｌ）可部分逆转ＡＣＴＨ的抑制作用，ｉ．ｔ．阿片受体阻断剂纳络酮（ＮＬＸ，１０μｇ）可部分逆转电针的抑制作用。结果提示ＡＣＴＨ和电针可能通过不同机制抑制甲醛痛敏大鼠脊髓ＮＯＳ阳性神经元增多。
In this paper, NADPH d histochemical staining technique to study the intrathecal injection (i.t.) ACTH and electroacupuncture stimulation (EA) on the increase of NOS-positive neurons in the spinal cord dorsal horn of rats with formaldehyde hyperalgesia. The results showed that ACTH (0.5U, i.t.) and electroacupuncture (1mA50Hz, 5mA5Hz, 1mA5Hz) could significantly inhibit the increase of NOS positive neurons in superficial layers of spinal dorsal horn after stimulating “Jiaji acupoint” for 30min; t. Inhibition was significantly increased when ACTH (0.5U) and EA stimulation (1mA5Hz) were administered simultaneously; i. t. NO precursor L-arginine (L Arg, 10nmol) can partially reverse the inhibitory effect of ACTH, i. t. The opioid receptor blocker naloxone (NLX, 10μg) partially reversed the inhibitory effect of electroacupuncture. The results suggest that ACTH and EA may inhibit the increase of NOS positive neurons in the spinal cord of rats with hyperalgesic pain through different mechanisms.