Uramoto H, Ohno T, Ishihara T
Laboratory of Experimental Pharmacology, Suntory Institute for Biomedical Research, Osaka, Japan.
Jpn J Pharmacol. 1990 Nov;54(3):287-98. doi: 10.1254/jjp.54.287.
We found that the gastric mucosal lesion induced by 60% ethanol containing 150 mM HCl was reduced by pre-loading the rat with restraint and water-immersion stress (22 degrees C). The resistance to ethanol injury was maximal in 1-hr stress loaded rats and gradually decreased with increasing time of stress (2-6 hr). The protective effect of stress was markedly decreased by subdiaphragmatic truncal vagotomy, and electrical stimulation of vagal nerves afforded similar protection as observed after stress. In contrast, pretreatment with atropine markedly reduced ethanol injury in both the control and 1 hr stress-loaded rats. One-hour stress produced surface epithelial cell damage in sham vagotomized rats, but the surface cells were almost intact in vagotomized rats. Pretreatment with indomethacin significantly mitigated the protective effect of stress against ethanol injury. However, the level of mucosal prostaglandin E2 was not changed 1 hr after stress, and it tended to decrease 6 hr after stress. Pretreatments with 1-hr stress and vagal stimulation weakly reduced localized staining of gastric mucosa with gentian violet. We conclude that adaptive protection can be achieved by restraint and water-immersion stress.
我们发现，通过对大鼠进行束缚和水浸应激（22℃）预处理，可减轻由含150 mM盐酸的60%乙醇诱导的胃黏膜损伤。在应激1小时的大鼠中，对乙醇损伤的抵抗力最大，且随着应激时间的增加（2 - 6小时）逐渐降低。膈下迷走神经切断术可显著降低应激的保护作用，而迷走神经电刺激提供的保护作用与应激后观察到的相似。相比之下，阿托品预处理在对照大鼠和应激1小时的大鼠中均显著减轻了乙醇损伤。1小时的应激在假迷走神经切断的大鼠中导致表面上皮细胞损伤，但在迷走神经切断的大鼠中表面细胞几乎完整。吲哚美辛预处理显著减轻了应激对乙醇损伤的保护作用。然而，应激1小时后黏膜前列腺素E2水平未发生变化，应激6小时后其水平有降低趋势。1小时的应激和迷走神经刺激预处理轻微降低了胃黏膜用龙胆紫的局部染色。我们得出结论，束缚和水浸应激可实现适应性保护。
