摘要
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。
The effects of intrathecally administrated (i.t.) atropine,glibenclamide,a blocker of ATPsensitive potassium channels,or naloxone on the antinociception produced by i.t. carbachol or morphine were observed and analyzed by an integrated EMG measurement of hindlimb flexor reflex in lightly pendarbitalanesthetized rats.The results showed that:i.t. carbachol produced a dosedependent antinociception;the antinociception produced by it. carbachol could be blocked dosedependently by i.t. naloxone or i.t. glibenclamide;the antinociception produced by i.t.morphine could also be blocked dosedependently by i.t.glibenclamide,but not by i.t.atropine.The results suggest that the antinociception produced by activation of muscarinic receptors at the spinal level might be mediated by endogenous opioids and ATPsensitive potassium channels in a cascade form.
出处
《山西医科大学学报》
CAS
1999年第2期97-100,共4页
Journal of Shanxi Medical University
基金
国家自然科学基金
