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阿斯匹林和其他非甾体类抗炎药可使实验动物和人的胃粘膜发生不同程度的损害和出血,其发生机制与胃酸有关。胃酸有助于药物以非离子弥散的形式进入胃粘膜细胞,导致细胞的渗透性、缓冲能力和代谢功能失调。阿斯匹林还能抑制前列腺素的合成;预先服用外源性前列腺素能防止阿斯匹林对胃粘膜的损害,因此该药的损害作用与胃粘膜内前列腺素缺乏有关。呋喃硝胺(ranitidine)是一种很有潜力的H_2受体阻滞剂。本文对前列腺素(PG)和呋喃硝胺的胃粘膜细胞保护作用进行了比较。方法:志愿受试者为8名健康无胃肠病的男性青年,按以下五种实验条件随机运用:1.安慰剂;2.阿斯匹林0.5g;3.PGE_20.5mg:4.呋喃硝胺10 mg;5.呋喃硝胺100mg。以上均为每日四次,后三组分别于每次服
Aspirin and other non-steroidal anti-inflammatory drugs can make experimental animals and human gastric mucosa damage and bleeding to varying degrees, the mechanism of occurrence of gastric acid. Stomach acid helps the drug enter the gastric mucosal cells in a non-ionic and diffuse fashion, resulting in cell permeability, buffering capacity, and metabolic dysfunction. Aspirin also inhibits the synthesis of prostaglandins; pre-administration of exogenous prostaglandins can prevent aspirin damage to the gastric mucosa, the drug’s damaging effects and the lack of prostaglandin in the gastric mucosa. Ranitidine is a promising H 2 blocker. This article compared prostaglandin (PG) and ranitidine in gastric mucosal cell protection. Methods: The volunteers were 8 healthy male volunteers with no gastrointestinal disease and were randomly assigned to the following five experimental conditions: 1. Placebo; 2. Aspirin 0.5g; 3. PGE 20.5mg: 4. Furan Nitramine 10 mg; 5. Furan nitramine 100 mg. The above are four times a day, after the three groups were in each service