Sütö G, Király A, Vincze A, Mózsik G
First Department of Medicine, Medical University, Pécs, Hungary.
Acta Physiol Hung. 1992;80(1-4):205-11.
It has been observed earlier that gastric cytoprotection produced by PGI2, beta-carotene, small doses of atropine or cimetidine has failed in surgically vagotomized rats. This phenomenon may be in connection with endogenous prostaglandins (PGs) and glutathione (GSH) level of the gastric mucosa. The aims of the study were to evaluate the effect of vagus nerve on the gastric mucosal 6-keto-PGF1 alpha, PGE2 and glutathione after intragastric 96% ethanol (ETOH) treatment. The observations were carried out on CFY rats. The gastric mucosal damage was produced by intragastric administration of 1 ml 96% ETOH. Acute bilateral surgical vagotomy (ASV) was carried out 30 min prior to ETOH application. The animals were sacrificed 1, 5, 15 or 60 min after ETOH installation. The number and the severity of gastric mucosal lesions were noted and 6-keto-PGF1 alpha, PGE2 an GSH contents of gastric mucosa were measured. It has been found that: 1. the number and the severity of gastric mucosal lesions were increased after ASV compared to those with intact vagal nerve, 2. 96% ETOH treatment increased both the gastric mucosal PGs and GSH levels, 3. 6-keto-PGF1 alpha peaked at 5 min PGE2 and GSH peaked at 15 min after ETOH treatment, 4. ASV decreased the gastric mucosal PGs content and delayed the peaks of PGE2 and GSH. It has been concluded that the decreased content of PGs and the delayed GSH increase may play a pathological role in the failure of gastric cytoprotection of rats after ASV.
早期研究发现，前列环素（PGI2）、β-胡萝卜素、小剂量阿托品或西咪替丁产生的胃细胞保护作用在手术切断迷走神经的大鼠中失效。这种现象可能与胃黏膜内源性前列腺素（PGs）和谷胱甘肽（GSH）水平有关。本研究旨在评估迷走神经对胃内给予96%乙醇（ETOH）后胃黏膜6-酮-前列腺素F1α（6-keto-PGF1α）、前列腺素E2（PGE2）和谷胱甘肽的影响。观察对象为CFY大鼠。通过胃内给予1 ml 96% ETOH造成胃黏膜损伤。在给予ETOH前30分钟进行急性双侧手术切断迷走神经（ASV）。在给予ETOH后1、5、15或60分钟处死动物。记录胃黏膜损伤的数量和严重程度，并测定胃黏膜中6-keto-PGF1α、PGE2和GSH的含量。结果发现：1. 与迷走神经完整的大鼠相比，ASV后胃黏膜损伤的数量和严重程度增加；2. 96% ETOH处理使胃黏膜PGs和GSH水平均升高；3. ETOH处理后，6-keto-PGF1α在5分钟达到峰值，PGE2和GSH在15分钟达到峰值；4. ASV降低了胃黏膜PGs含量，并延迟了PGE2和GSH的峰值出现时间。研究得出结论，PGs含量降低和GSH升高延迟可能在ASV后大鼠胃细胞保护作用失效中起病理作用。
