Effects of Thiocyanate and Acetylsalicylic Acid on the Gastric Mucosal Barrier in Rats

Abstract

The proposed presence of the gastric mucosal barrier system, which interferes with the back diffusion of hydrogen ion secreted in gastric juice (1), has been postulated to protect the possible occurrence of mucosal damage due to hydrochloric acid (2). Though the precise nature of the barrier remains biochemically unknown, mucous substances covering the mucous layer or mucosal epithelical cells are indicated to be related with barrier function (3).<BR>Occurrence of the back diffusion of hydrogen ion in association with the equivalent increase in the intraluminal efflux of sodium ion in the surgically or pharmacologically vagotomized stomach of the rat or the dog indicated the equilibrated exchanges of hydrogen and sodium ions across the mucous epithels (4, 5).<BR> Increase in the back diffusion of hydrogen ion by thiocyanate (2) and acetazolamide (6) in the vagotomized dog stomach suggests an essential role of a carbonic anhydrase in the maintenance of the gastric mucosal barrier, as the enzyme is present in the gastric mucosa and activity is inhibited by both agents.<BR> Though thiocyanate as one of non-anticholinergic antacids has been an available pharmacological tool for elucidation of the mechanism of gastric acid secretion, especially in the gastric mucosa of frog in vitro, many discussions have been presented on the mode of its action (7-9).<BR> Marked inhibition of the gastric acid secretion without affecting the volume of gastric juice by thiocyanate in the oral route prompted the study of the correlation between the inhibitory effect and increase in the back diffusion of hydrogen ion by thiocyanate. METHODSI. Sampling the gastric juice in rats Male SD rats, 7 to 8 weeks of age and fasted previously for approx. 18 hr, were an esthetized with ether. The animals were divided into groups of 5. Exposition of the pyloric region of the stomach through abdominal incision along the middle line was followed by the ligation of the pylorus. Immediately thereafter, 2 ml of physiological saline was injected s.c. in order to prevent dehydration. Five hr after surgical pro cedures, the animals were sacrificed under deep ether anesthesia in order to extirpate the whole stomach. The volume (ml), hydrogen ion concentration and pepsin activity in the

Effect of geranylgeranylacetone (GGA) on gastric lesions induced by topical aspirin plus HCl.

“…In addition, volume, H+ concentration, Na+ concentration, and pepsin output in the collected gastric juice were unchanged in any group (Table 2). This result suggests that the back diffusion of H+ ion from the lumen to the mucosa might be involved in the aggravation of the lesions by aspirin or other mucosal barrier breakers, since the changes of electrolytes did not yet occur in a short period (2 hr after the aspirin-treatment), while the decrease of H+ concentration and the increment of Na+ concentration were observed 3 hr or more later after the aspirin treatment (11,14,15).…”