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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.

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