Acid-induced gastric damage in rats is aggravated by starvation and prevented by several nutrients.

The aggravation of acid-induced gastric damage and its prevention by glucose, ascorbate or glutathione precursors was studied in fed and food-deprived rats. The stomachs of fed rats and those starved for 1, 3 or 5 d were vagotomized just before irrigating for 3 h with solutions containing 0-150 mmol HCI/L. Mucosal glutathione, mucus, lipid peroxides and acid back-diffusion were measured. Stomach ulcers were evaluated by morphological and histological examination. The preventive effects of glucose, ascorbate and a mixture of L-glutamine, L-glycine and L-cysteine were evaluated in the stomachs of rats that were starved for 5 d, vagotomized, then perfused for 3 h with 100 mmol HCI/L. Greater acid back-diffusion and ulcer formation, and lower glutathione and mucus levels in starved rats were dependent on the duration of starvation and luminal acidity. Increased acid back-diffusion and decreased glutathione and mucus production were negatively correlated (r < -0.80, P < 0.05) with ulcer formation. A significant enhancement in mucosal lipid peroxide concentration and serious damage of forestomach and corpus mucosal cells were observed in starved rats exposed to 100 mmol HCI/L. These ulcerogenic factors were effectively inhibited in acid-perfused stomachs of food-deprived rats by daily intraperitoneal injection of the amino acid mixture (150 mg/kg) or by an average daily consumption via drinking water of glucose (10 g) or ascorbate (1.2 g). Starvation aggravated acid-induced gastric damage and was associated with greater acid back-diffusion and oxygen radical generation, and lower mucosal glutathione and mucus production.

Prophylactic effects of sucralfate and geraniin on ethanol-induced gastric mucosal damage in rats.

The aim is to study the protective effects of topical sucralfate and geraniin on acidified ethanol (EtOH dissolved in 100 mM HCI plus 54 mM NaCl)-induced gastric acid back-diffusion, mucus production and mucosal ulcerations in the rat. After irrigation the stomach with acidified EtOH (10-40% v/v) for 3 hrs, a concentration-dependent increase in acid back-diffusion and in mucosal lesions, and -dependent reduction in mucus production was found. These ulcerogenic effects of EtOH were dose-relatedly inhibited by pretreatment of intragastric sucralfate (10-200 mg/kg). A high correlation (r = -0.9572) between sucralfate-induced inhibition in acid back-diffusion and -induced reduction in mucosal ulceration provoked by 30% EtOH was observed. Geraniin (10-100 mg/kg), given 30 min prior to EtOH perfusion, produced potent inhibitory effects on those ulcerogenic parameters provoked by EtOH in a dose-dependent manner. The correlation (r = -0.8638) between geraniin-induced inhibitions in acid back-diffusion and in mucosal ulceration produced by EtOH was achieved. These cytoprotective effects of sucralfate and geraniin were further confirmed by morphological and histological studies. The results suggested that the protective effects of sucralfate and geraniin on gastric mucosa against acidified EtOH-induced damage are at least partly through the inhibition in acid back-diffusion and the elevation of gastric mucus production.