【摘要】 1.给大鼠脊髓蛛网膜下腔注射甲啡肽200—800nmol引起与剂量相关的镇痛效应。注射脑啡肽降解酶抑制剂Thiorphan 50nmol或Benatin 300nmol可加强电针镇痛,注射甲啡肽抗体则可对抗电针镇痛。这些资料说明内源性甲啡肽确实在痛觉调制系统中起着重要作用。 2.脊髓蛛网膜下腔注射亮啡肽800nmol使痛阈升高44％,其镇痛效应尚不及200nmol甲啡肽的作用(痛闻升高61％);注射甲七肽10-200nmol未见痛阈明显改变。注射亮啡肽或甲七肽抗体并不能对抗电针镇痛;注射甲七肽降解酶抑制剂Captopril 1000nmol也不能加强电针镇痛。这些资料说明,脊髓中的亮啡肽和甲七肽存痛觉调制中可能不起重要作用。更多还原

【Abstract】 1. Intrathecal injection of Met-enkephalin (200, 400 and 800 nmol) in rats produced a dose-dependent analgesic effect. That the effect of electroacupuncture (EA) analgesia could be markedly potentiated by ivtrathecal injection of bestatin or thio-phan, the enkephalin degrading enzyme inhibitors, and attenuated by the Met-enkephalin. antiserum strongly suggest the importance of endogenous Met-enkephalin in the pain modulatory system.2. Intrathecal injection of Leu-enkephalin 800 nmol produced only a slight increase of tail flick latency (44±13%) comparable to 200 nmol of Met-enkephalin (61±27%). No significant analgesic effect was seen when Met-enkephalin-Arg6-Phe7 (MBAP) 10-200 nmol was injected intrathecally to the rat. The effect of EA analgesia was not significantly attenuated by intratbecal injection of antisera against Leu-enkephalin or MEAP, nor was it potentiated by captopril (240 nmol), the inhibitor of the HEAP degrading enzyme. All these evidences seem to point to the conclusion that Leu-enkephalin and MEAP in the spinal cord may not play important role in the modulation of pain perception.更多还原