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首页> 外文期刊>Japanese Journal of Pharmacology >ACID BACK-DIFFUSION AND MUCOSAL H+ HANDLING IN THE RAT STOMACH UNDER NORMAL AND STRESS-INDUCED CONDITIONS
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ACID BACK-DIFFUSION AND MUCOSAL H+ HANDLING IN THE RAT STOMACH UNDER NORMAL AND STRESS-INDUCED CONDITIONS

机译:正常和应力诱导条件下大鼠胃酸回扩散和粘膜H +处理

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References(25) Cited-By(4) 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 outputet flux of H+ was significantly increased by stress. Thus, (1) spontaneous acid backdiffusion 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.
机译:参考文献(25)By-By(4)在正常和压力诱发的条件下,将盐酸滴入胃中后,我们同时测定了迷走神经切断的大鼠的胃酸反扩散和胃蛋白酶输出。在两种条件下,暴露于6 ml的100 mM HCl中,自发酸反扩散都随实验的进行而增加,并且由于压力,酸反扩散的幅度显着降低。胃蛋白酶的产量没有变化。虽然阿司匹林或牛磺胆酸引起的腔酸消失不会因压力而改变,但应激大鼠的胃蛋白酶对H +的输出却显着增加。在两种条件下,暴露于各种浓度的HCl 3小时后,腔酸的消失随HCl的浓度线性增加。在正常条件下,除浓度为300 mM以外,酸的反向扩散幅度是三倍,并且由于压力,胃蛋白酶输出/ H +净通量之比显着增加。因此,(1)自发酸的反扩散随着应力而降低,而化学屏障破坏剂引起的扩散保持不变; (2)H +扩散回到粘膜的作用并不总是与由管腔中H +的损失确定的扩散量平行; (3)正常黏膜中黏膜内H +可能大部分消散; (4)压力引起的药物诱导的粘膜损伤的发生或加剧可能与H +耗散机制不足有关。

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