Bovill J G
Department of Anaesthesiology, University Hospital Leiden, The Netherlands.
Eur J Anaesthesiol Suppl. 1997 May;15:9-15. doi: 10.1097/00003643-199705001-00003.
Opioids and non-steroidal anti-inflammatory drugs (NSAIDs) are the commonest drugs used to treat pain. Opioids mimic the actions of endogenous opioid peptides by interacting with mu, delta or kappa opioid receptors. The opioid receptors are coupled to G1 proteins and the actions of the opioids are mainly inhibitory. They close N-type voltage-operated calcium channels and open calcium-dependent inwardly-rectifying potassium channels. This results in hyperpolarization and a reduction in neuronal excitability. They also decrease intracellular cAMP which modulates the release of nociceptive neurotransmitters (e.g. substance P). Inhibition of prostaglandin synthesis by cyclooxygenase is the principal mode of the analgesic and anti-inflammatory actions of NSAIDs. Cyclo-oxygenase is inhibited irreversibly by aspirin and reversibly by other NSAIDs. The widespread inhibition of cyclo-oxygenase is responsible for many of the adverse effects of these drugs. NSAIDs also reduce prostaglandin production within the CNS. This is the main action of paracetamol.
阿片类药物和非甾体抗炎药（NSAIDs）是治疗疼痛最常用的药物。阿片类药物通过与μ、δ或κ阿片受体相互作用来模拟内源性阿片肽的作用。阿片受体与G1蛋白偶联，阿片类药物的作用主要是抑制性的。它们关闭N型电压门控钙通道并打开钙依赖性内向整流钾通道。这导致超极化并降低神经元兴奋性。它们还减少细胞内cAMP，后者调节伤害性神经递质（如P物质）的释放。环氧化酶抑制前列腺素合成是NSAIDs镇痛和抗炎作用的主要方式。阿司匹林不可逆地抑制环氧化酶，其他NSAIDs则可逆地抑制。环氧化酶的广泛抑制是这些药物许多不良反应的原因。NSAIDs还减少中枢神经系统内前列腺素的产生。这是对乙酰氨基酚的主要作用。
