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采用记录大鼠伤害性屈肌反射积分肌电图的方法，观察了鞘内注入Ｃａｒｂａｃｈｏｌ（Ｃａｒ，胆硷能Ｍ受体激动剂）及吗啡引起的抗痛作用，并分析了纳洛酮（μ受体阻断剂）、优降糖（ＫＡＴＰ通道阻断剂）及阿托品对上述药物抗痛作用的影响，结果显示：①鞘内注入Ｃａｒ引起剂量依赖性的抗痛作用；②Ｃａｒ的抗痛作用可被鞘内予先注入纳洛酮或优降糖阻断；③鞘内注入吗啡引起的抗痛作用可被优降糖阻断，但不能被阿托品所阻断。这些结果提示：内源性阿片肽和ＫＡＴＰ通道介导了Ｃａｒ或乙酰胆硷引起的脊髓抗痛作用，在此过程Ｍ受体的激活引起内源性阿片肽的释放，后者通过打开ＫＡｒｐ通道实现镇痛。
Using the method of recording the EMG of rat nociceptor reflex, we observed the intrathecal injection of Carbachol (Car, cholinergic M receptor agonist) and morphine-induced analgesic effects. The effects of naloxone (μ Receptor blockers), glyburide (KATP channel blockers) and atropine on the anti-pain effect of the above drugs, the results showed: ① intrathecal injection of Car induced a dose-dependent anti-pain effect; ② Carb analgesic effect Can be pre-intrathecal injection of naloxone or hypoglycemic block; ③ intrathecal morphine-induced analgesic effect can be hypoglycemic block, but can not be blocked by atropine. These results suggest that endogenous opioid peptides and KATP channels mediate carotid or acetylcholine-induced spinal analgesia in which activation of M receptors results in the release of endogenous opioid peptides, which are activated by opening the KArp channel Achieve pain relief.