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本文首次报告,将强啡肽注入大鼠脊髓蛛网膜下腔有强烈而持久的镇痛作用。用辐射热甩尾阈升高幅度和镇痛时程为指标,强啡肽镇痛作用在2.3—18.6毫微克分子范围内呈明确的剂量效应关系。若以等克分子计算,较吗啡的镇痛作用强6—10倍,较另一μ型阿片受体激动剂morphiceptin强65—100倍。应用强啡肽抗血清中提出的免疫球蛋白G可以完全对抗强啡肽的镇痛作用。纳洛酮也可对抗强啡肽镇痛,但作用慢而弱。在急性吗啡耐受的大鼠,强啡呔的镇痛作用依然存在,说明两者不产生交叉耐受。多方面的资料表明,强啡肽在脊髓的镇痛作用可能是通过k型阿片受体而实现的。与脊髓内注射不同,脑室内注射强啡肽并无镇痛作用。 相似文献
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Evidences are presented to show a strong and long-lasting analgesic effect after injec-tion of dynorphin into the subarachnoid space of the spinal cord in the rat. Taking theamplitude and time course of the increase of tail flick latency as the indices of analgesia,dynorphin elicited dose-dependent analgesic effect in the range of 2.3--18.6 nmol. Calcu-lating on a molar basis dynorphin was 6--10 times more potent than morphine and 65--100 times more potent than morphiceptin, another mu opiate receptor agonist. Dynorphinanalgesia was completely reversed by intrathecal injection of anti-dynorphin IgG and par-tially reversed by naloxone. Acute tolerance to morphine analgesia did not affect the occu-rance of dynorphin analgesia, indicating the absence of cross tolerance between morphineand dynorphin. Evidence from different lines of approach suggests that dynorphin may bindwith kappa opiate receptors in the spinal cord to exert its analgesic effect 相似文献
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大鼠脊髓蛛网膜下腔注射去甲肾上腺素引起中枢性降压效应,此效应可被a受体阻断剂酚妥拉明、哌唑嗪或育亨宾所拮抗,但不受β阻断剂心得安、Metoprolol或Butoxamine的影响。强啡肽抗体或大剂量纳洛酮也可对抗去甲肾上腺素或a受体激动剂可乐宁的心血管抑制效应;而β-内啡肽、甲啡肽与亮啡肽抗体以及小剂量纳洛酮均无拮抗作用。蛛网膜下腔注射强啡肽可引起与剂量相关的降压效应。以上结果提示,脊髓蛛网膜下腔注射去甲肾上腺素的降压效应与脊髓内a受体的激活以及内源性强啡肽的释放有关。 相似文献
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