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非类固醇抗炎药(NSAID)按属性分类是开处方最多的一类药物。所有的NSAID均会损伤胃十二指肠粘膜,服用后短至24h就会出现显著的损伤。,此时口服消炎痛的损伤程度达到峰值。治疗量的消炎痛可增加基础的和刺激的胃酸分泌量,这可能是通过抑制前列腺素的产生而实现的。前列腺素能抑制肥大细胞释放介质,而消炎痛能逆转这种作用。肥大细胞是胃内组织胺的主要来源,并参与乙醇和NSAID引起的粘膜损伤反应。甲哌噻庚酮(ketotifen)已用于长程治疗哮喘,变态反应性和过敏性疾病。其主要作用方式是阻断肥大
Non-steroidal anti-inflammatory drugs (NSAIDs) are the most prescribing drugs by attribute. All NSAIDs can damage the gastroduodenal mucosa, and significant damage can occur as soon as possible after 24 hours. At this point the degree of damage to oral indomethacin peaked. Indomethacin at a therapeutic level increased basal and stimulated gastric acid secretion, probably by inhibiting prostaglandin production. Prostaglandins inhibit mast cell release mediators, whereas indomethacin reverses this effect. Mast cells are the major source of histamine in the stomach and are involved in the mucosal injury response to ethanol and NSAIDs. Ketotifen has been used for long-term treatment of asthma, allergic and allergic diseases. Its main mode of action is to block the hypertrophy