Hough L B, Glick S D, Su K
Life Sci. 1985 Mar 4;36(9):859-66. doi: 10.1016/0024-3205(85)90210-3.
Scrambled DC current applied to the hind paws of rats caused an analgesic response that was inhibited by the histamine H2-receptor antagonists cimetidine, ranitidine and oxmetidine, but not by high doses of naloxone (the opiate antagonist), or other transmitter receptor antagonists. In contrast, AC current applied to all paws produced analgesia that was blocked by naloxone, but not cimetidine, showing the independence of these systems. These findings indicate a specific role for histamine and H2-receptors as mediators of endogenous non-opiate analgesia. In addition, a combination of cimetidine and naloxone did not abolish either form of footshock analgesia, implying the existence of a non-opiate, non-H2, endogenous pain-relieving system. These results also suggest that drugs capable of penetrating the brain and stimulating H2-receptors might have analgesic properties.
施加于大鼠后爪的不规则直流电会引起镇痛反应，该反应会被组胺H2受体拮抗剂西咪替丁、雷尼替丁和奥美替丁抑制，但不会被高剂量的纳洛酮（阿片类拮抗剂）或其他递质受体拮抗剂抑制。相比之下，施加于所有爪子的交流电产生的镇痛作用会被纳洛酮阻断，但不会被西咪替丁阻断，这表明这些系统是独立的。这些发现表明组胺和H2受体作为内源性非阿片类镇痛介质具有特定作用。此外，西咪替丁和纳洛酮的组合并没有消除任何一种形式的足部电击镇痛，这意味着存在一种非阿片类、非H2的内源性疼痛缓解系统。这些结果还表明，能够穿透大脑并刺激H2受体的药物可能具有镇痛特性。
