Abstract
The etiology of atrophic gastritis has not been established. Although the circulating antibody to a constituent of the gastric parietal cell has been demonstrated in a large number of patients with pernicious anemia and atrophic gastritis (1-5), the significance of the parietal cell antibody in causing or perpetuating any type of chronic gastritis is unknown. Jacob and Glass (6) have presented direct evidence that the parietal cell antibody is a complement fixing antibody, and have supported the concept that the autoimmune mechanism participates in the development of the gastric atrophic lesion in a proportion of patients with pernicious anemia and atrophic gastritis. Fiasse et al. (7) failed to show inhibition of gastric secretion after a single injection of human parietal cell antibody in the rat. On the other hand, Tanaka and Glass (8) have reported that rats injected with human parietal cell antibody for 6 to 8 weeks showed a profound decrease of hydrochloric acid output, and had mild atrophic lesions in the gastric mucosa. Hausamen et al. (9) have shown that the injection of rabbit antisera against antigens from guinea pig gastric mucosa into guinea pigs, resulted in an acute inflammation confined to the stomach. In the present study, shortand long-term effects of rabbit antibodies against rat gastric mucosa and gastric juice on gastric secretion in the rat, were investigated.
