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正常及应激诱导条件下大鼠胃内的酸反向扩散及黏膜氢离子处理

Acid back-diffusion and mucosal H+ handling in the rat stomach under normal and stress-induced conditions.

作者信息

Takeuchi K, Okabe S

出版信息

Jpn J Pharmacol. 1983 Feb;33(1):85-93. doi: 10.1254/jjp.33.85.

Abstract

We determined acid back-diffusion and pepsin output simultaneously in vagotomized rats after instillation of HCl into the stomach under normal and stress-induced conditions. With exposure to 6 ml of 100 mM HCl, spontaneous acid back-diffusion increased with the duration of the experiment under both conditions, and the magnitude of the acid back-diffusion was decreased significantly by stress. There was no change in the output of pepsin. While disappearance of luminal acid caused by aspirin or taurocholic acid was not altered by stress, the pepsin output in response to H+ increased significantly in the stressed rats. With exposure to various concentrations of HCl for 3 hr, disappearance of the luminal acid increased linearly with the grade of HCl under both conditions. Except for the concentration of 300 mM, the magnitude of the acid back-diffusion was triple in the normal condition, and the ratio of pepsin output/net flux of H+ was significantly increased by stress. Thus, (1) spontaneous acid back-diffusion decreased with stress, while diffusion induced by chemical barrier breakers remained the same; (2) the action of H+ diffused back into the mucosa did not always parallel the amount of diffusion determined from the loss of H+ in the lumen; (3) intramucosal H+ may be largely dissipated in normal mucosa; and (4) the initiation or aggravation of drug-induced mucosal damages by stress may be related to insufficiency of the H+ dissipating mechanisms.

摘要

我们在正常和应激诱导条件下,向迷走神经切断的大鼠胃内滴注盐酸后,同时测定了酸反向扩散和胃蛋白酶分泌量。给予6毫升100毫摩尔/升盐酸后,在两种条件下,自发性酸反向扩散均随实验时间延长而增加,且应激可显著降低酸反向扩散的幅度。胃蛋白酶分泌量无变化。虽然阿司匹林或牛磺胆酸引起的腔内酸消失不受应激影响,但应激大鼠中对H⁺反应的胃蛋白酶分泌量显著增加。给予不同浓度盐酸3小时后,在两种条件下,腔内酸的消失均随盐酸浓度升高呈线性增加。除300毫摩尔/升浓度外,正常条件下酸反向扩散幅度增加两倍,应激可显著增加胃蛋白酶分泌量/H⁺净通量的比值。因此,(1)自发性酸反向扩散随应激降低,而化学屏障破坏剂诱导的扩散保持不变;(2)扩散回黏膜的H⁺的作用并不总是与根据腔内H⁺损失确定的扩散量平行;(3)黏膜内H⁺在正常黏膜中可能大量消散;(4)应激导致药物性黏膜损伤的起始或加重可能与H⁺消散机制不足有关。

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