电刺激束缚小鼠应激诱发胃溃疡及其机制的初步探讨

THE PRIMARY PROBE OF GASTRIC ULCER INDUCED BY ELECTRIC STIMULUS RESTRAINT STRESS IN MICE

用电刺激躯体束缚小鼠的口唇部建立应激性胃溃疡模型，以阿尔新兰－ＭｇＣｌ２洗脱法测定胃壁粘液量．研究安定、苯巴比妥钠、可的松、酚妥拉明、异丙肾上腺素、阿托品和乙醇对溃疡发生的影响．结果表明，安定、苯巴比妥钠和异丙肾上腺素显著抑制溃疡发生；阿托品和乙醇可明显使溃疡加剧；酚托拉明和可的松对溃疡没有影响．模型动物胃壁粘液量与对照组比较以及所有药物对模型动物胃壁粘液量却没有明显变化．提示，电刺激束缚应激胃溃疡的发生与削弱胃粘液屏障无关．

The paper efficiently established the stress ulcer model by electric stimulus on mouth lip site of body restraint mouse, estimated the mucus quantity of stomach wall by means of the Alcian blue MgCL 2 rins, and probed the effects of diazepam,sodium phenobarbital,cortisone ,phentolamine, isoproterenol,atropine and ethanol on development of the ulcer . The results showed that diazepam, sodium phenobarbital and isoproterenol significant ly inhibited the ulcer. Whereas atropine and ethanol markedly exacerbated theulcer, but phentolamine and cortisone had no notable effect on the ulcer. There was no significant difference between the mucus quantity of stomach wall in both model animals and that in normal animals ,and all of used drugs did not change the mucus quantity of stomach wall in the model animals. These results suggested that the development of ERSU had no relation to weakening gastric mucus barrier.The ulceration of ERS was evoked via CNS, possibly it was the principal mechanism of ERSU that ERS changed the functon of CNS ,thereby affected the activity of vagus nerve and resulted in constriction of gastric blood vessels and blockade of gastric microcirculation.