胃黏膜对阿司匹林适应性的实验研究

An experimental study on gastric adaptation to aspirin in rats

目的 探讨胃黏膜对阿司匹林的适应性及其发生机制。方法 连续数天经胃管给大鼠灌入酸化阿司匹林 (acidifiedaspirin ,ASA) ,计算胃黏膜损伤面积和损伤深度。用RIA法检测胃黏膜组织内EGF的含量。为观察一氧化氮 (NO)在胃黏膜对ASA适应性中的作用 ,在应用ASA前 30min经大鼠尾静脉分别注入L 精氨酸 (Arg)、L NAME及L Arg +L NAME ,观察胃黏膜损伤面积及深度。 结果 初次应用ASA ,大鼠胃黏膜损伤面积为 (5 0 .4± 6 .2 )mm2 ,随着ASA继续应用 ,损伤面积逐渐减轻 ,P<0 .0 1。胃黏膜组织内EGF含量逐渐增加 ,P <0 .0 1。应用L Arg、L NAME及L Arg +L NAME后 ,大鼠胃黏膜对ASA的适应性依然存在 ,但L NAME组损伤面积重于L Arg组 ,P <0 .0 1。 结论 大鼠胃黏膜对阿司匹林具有适应性 ,其完全适应时间为 4d。其适应的可能机制之一是胃黏膜组织内EGF含量增加。NO在胃黏膜对阿司匹林的适应性中起一定作用 ,抑制其合成后 。

Objective To investigate the gastric adaptation to aspirin in rats. Methods Mucosal injury was induced by repeated doses of acidified aspirin (ASA) in rats. Mucosal lessions and necrosis depth were measured. Mucosal contents of epidermal growth factor (EGF) were tested by radioimmunoassay. To test the possible implication of endogenous nitric oxide in gastric adaptation to aspirin. L Arg, L NAME and L Arg+L NAME were given intravenously 30 minutes before the exposure to ASA. Results The lession areas of gastric mucosa in first exposure to ASA was (50.4±6.2)mm 2. After repeated dose of ASA, the mucosal lessions were significantly alleviate, P <0.01. The mucosal contents of EGF were significantly increased, P <0.01. The rat mucosa had adaptation to ASA after pretreated L Arg、L NAME and L Arg+L NAME. The lession areas of the pretreated L NAME rats were significantly bigger than that of the pretreated L Arg rats. Conclusion Gastric mucosa exhibits the ability to adapt to ulcerogenic action of aspirin. After four days repeated doses of ASA, the full adaptation to ASA was achieved. The mechanism of the adaptation was possibly through increased gastric mucosal EGF. NO played a part of role in the gastric adaptation to ASA.