Ferreira S H
Br J Clin Pharmacol. 1980 Oct;10 Suppl 2(Suppl 2):237S-245S. doi: 10.1111/j.1365-2125.1980.tb01806.x.
1 Prostaglandins released by tissue injury sensitize nociceptors and produce hyperalgesia. 2 Aspirin-like drugs inhibit prostaglandins I2 and E2, synthesis, which explains their anti-algic effect. 3 The anti-algic effect of aspirin-like drugs in carrageenin-induced rat paw inflammation may involve a central component. 4 Prostaglandin E2-induced hyperalgesia, once established, is not relieved by systemically administered drugs. 5 Prostaglandin-induced hyperalgesia is possibly a cyclic adenosine, 3',5'-monophosphate C2+ dependent process. 6 Morphine, enkephalins, opiate antagonists and cyclic guanosine 3',5'-monophosphate have a peripheral analgesic effect in the prostaglandin hyperalgesia test. 7 Morphine may produce peripheral analgesia by inhibiting adenylatecyclase activity at the nociceptors.
组织损伤释放的前列腺素使伤害感受器敏感化并产生痛觉过敏。
阿司匹林类药物抑制前列腺素I2和E2的合成,这解释了它们的抗痛觉过敏作用。
阿司匹林类药物对角叉菜胶诱导的大鼠爪部炎症的抗痛觉过敏作用可能涉及中枢成分。
一旦建立,前列腺素E2诱导的痛觉过敏不会因全身给药而缓解。
前列腺素诱导的痛觉过敏可能是一个依赖环磷酸腺苷(cAMP)和钙离子的过程。
在前列腺素痛觉过敏试验中,吗啡、脑啡肽、阿片拮抗剂和环磷酸鸟苷具有外周镇痛作用。
吗啡可能通过抑制伤害感受器处的腺苷酸环化酶活性产生外周镇痛作用。