Wörner Jakobea, Rukwied Roman, Konrad Christoph
Institut für Anästhesie, chirurgische Intensivmedizin, Rettungsdienst und Schmerztherapie, Kantonsspital Luzern.
Anasthesiol Intensivmed Notfallmed Schmerzther. 2009 Nov;44(11-12):736-44. doi: 10.1055/s-0029-1242128. Epub 2009 Nov 16.
The sensation of pain arises through stimulation of peripheral nociceptors and is transmitted centrally involving several receptors and ion channels. In addition many endogenous physiologic pain-modulating mechanisms exist. Besides of classical analgesics, numerous other drugs showed analgesic properties based on diverse modes of actions along the pain pathway. These co-analgesics, administered in combination with classical drugs, are able to reduce painful states of different origin. We describe the peripheral action sites of co-analgesics, such as cannabinoids, capsaicin, bisphosphonates, steroids and somatostatin. We also summarise the effect of peripherally and centrally acting ion-channel blockers, e.g. local anaesthetics, carbamazepine and tolperisone working on sodium channels and gabapentin and pregabalin working on calcium channels. Finally, central analgesic mechanisms are discussed, for instance the inhibition of NMDA-receptors by ketamine or magnesium, the stimulation of alpha2-receptors by clonidine, tizanidine or antidepressants, the activation of GABA-receptors through baclofen and other analgesic mechanisms of i.e. ondansetron and neostigmine.
疼痛的感觉通过外周伤害感受器的刺激产生,并通过涉及多种受体和离子通道的方式向中枢传导。此外,还存在许多内源性生理疼痛调节机制。除了经典镇痛药外,许多其他药物基于疼痛通路中不同的作用方式也显示出镇痛特性。这些辅助镇痛药与经典药物联合使用,能够减轻不同来源的疼痛状态。我们描述了辅助镇痛药的外周作用部位,如大麻素、辣椒素、双膦酸盐、类固醇和生长抑素。我们还总结了外周和中枢作用的离子通道阻滞剂的作用,例如作用于钠通道的局部麻醉药、卡马西平和托哌酮,以及作用于钙通道的加巴喷丁和普瑞巴林。最后,讨论了中枢镇痛机制,例如氯胺酮或镁对NMDA受体的抑制、可乐定、替扎尼定或抗抑郁药对α2受体的刺激、巴氯芬对GABA受体的激活,以及昂丹司琼和新斯的明等其他镇痛机制。