Figler M, Szabó I, Mózsik G
First Department of Medicine, University Medical School of Pécs, Hungary.
J Physiol Paris. 1999 Dec;93(6):495-9. doi: 10.1016/s0928-4257(99)00111-4.
The aim of this study was to evaluate the effects of intragastrically given pectin-induced physicochemical properties and actions on active gastric acid secretion and on the development of ethanol- and aspirin-induced gastric mucosal lesions. The observations were carried out on CFY-strain rats, fasted for 24 h before the experiments with water ad libitum. The observations were carried out in two experimental series. A) The gastric mucosal lesions were produced by intragastrically given 96% ethanol or aspirin prepared with 0.2 M HCl. Different doses of pectin (100, 50 and 25 mg x kg(-1), respectively) were administered intragastrically 30 min before giving necrotizing agents. The number of gastric lesions was noted 1 h after the administration, while the severity of gastric mucosal lesions was scored by semi-quantitative scale. B) The effects of pectin were studied on the volume and H+ secretion of the stomach in 4-h pylorus-ligated rats. It has been found that: 1) the gastric mucosal lesions could be produced in 100% of rats by the application of both necrotizing agents. 2) Pectin in doses of 50-100 mg x kg(-1) increased the number of gastric mucosal lesions in both models, while no increase was produced by the application of 25-mg x kg(-1) dose. 3) The severity of mucosal lesions increased significantly after the administration of all doses of pectin. 4) The pectin-induced increase of gastric lesions (number) showed a dose-response effect. 5) The pectin produced a significant increase in the volume of gastric secretion and gastric H+ secretion. It has been concluded that: a) pectin-induced physicochemical changes are able to enhance the aggression to gastric mucosa produced by ethanol and aspirin; b) a positive correlation exists between the linkage of H+ to pectin and significant active metabolic response in the rat stomach; c) pectin alone stimulates the active metabolic process of the gastric H+ secretion.
本研究的目的是评估胃内给予果胶所诱导的物理化学性质及作用，及其对胃酸分泌活性以及乙醇和阿司匹林诱导的胃黏膜损伤形成的影响。观察对象为CFY品系大鼠，实验前禁食24小时，自由饮水。观察分两个实验系列进行。A）通过胃内给予用0.2 M盐酸配制的96%乙醇或阿司匹林来造成胃黏膜损伤。在给予坏死剂前30分钟，胃内分别给予不同剂量的果胶（分别为100、50和25 mg·kg⁻¹）。给药1小时后记录胃损伤数量，同时用半定量量表对胃黏膜损伤的严重程度进行评分。B）研究果胶对幽门结扎4小时大鼠胃的容积和H⁺分泌的影响。结果发现：1）两种坏死剂均可使100%的大鼠产生胃黏膜损伤。2）50 - 100 mg·kg⁻¹剂量的果胶增加了两种模型中胃黏膜损伤的数量，而25 mg·kg⁻¹剂量则未增加。3）所有剂量的果胶给药后，黏膜损伤的严重程度均显著增加。4）果胶诱导的胃损伤数量增加呈现剂量反应效应。5）果胶使胃分泌量和胃H⁺分泌量显著增加。研究得出以下结论：a）果胶诱导的物理化学变化能够增强乙醇和阿司匹林对胃黏膜的侵袭作用；b）H⁺与果胶的结合与大鼠胃中显著的活跃代谢反应之间存在正相关；c）单独的果胶可刺激胃H⁺分泌的活跃代谢过程。
