Migration of acetic acid and sodium acetate and their effects on the gastric transmucosal ion exchange.

Abstract

AbstractThe kinetics of the disappearance of acetic acid and sodium acetate from the stomach during secretion and secretory arrest was studied in anesthetized cats. Model experiments were also performed in which the solutes diffused through a cellophane membrane. On instillation of acetic acid into non‐secreting stomachs, the hydrogen ion concentration decreased significantly more rapidly than the acetate concentration (p<0.05). The increase in the combined sodium and potassium ion concentrations was significantly greater than the increase in the chloride ion concentration. Thus, in addition to molecular diffusion of acetic acid, exchange diffusion took place between hydrogen ions and sodium ions. A small amount of secretion masked this exchange. The acetate disappeared more rapidly on instillation of acetic acid than on installa‐. tion of sodium acetate. Acetic acid increases the ionic permeability of the gastric mucosa and has inhibitory effect on secretion. It has been reported that this secretory inhibition persists for up to 24 hrs. By repeated instillation experiments in the cat it was found that the permeability effects of a 30 min installation of 170 mM acetic acid did not persist for longer than 90 min. Sodium acetate per se probably had no effect on the ionic permeability of the gastric mucosa. It is suggested that the permeability increasing effect of acetic acid is related to transient intracellular accumulation of the diffusing acid. Epithelial abrasion that would give rise to an increased permeability by decreasing the diffusion distance requires restoration of the surface epithelium within 90 min and in fact, no abrasion was observed as an affect on acetic acid on the mucosa.