Cell proliferation in the gastric epithelium of the ulcer rat

Abstract

Objective. Cell division is brisk in the ulcer margin and many of the new cells will migrate over and cover the ulcer bed. The aim of this study was to determine how agents that promote or delay gastric ulcer healing influence cell proliferation in the gastric epithelium. Material and methods. Acetic acid ulcers were produced in the rat gastric corpus; non-ulcer rats served as controls. All rats were given a continuous infusion of ³H-thymidine. Some rats were also given gastrin or indomethacin, or infected with Helicobacter pylori. The rats were killed after 1, 2, 6 or 13 days, and the ulcer margin and undamaged corpus were excised for determination of labeling index (LI) by autoradiography. Antrum, duodenum and colon were also studied. Silver grain counting was carried out in some groups. Results. LI in the ulcer margin grew exponentially, reaching 84% after 6 days; gastrin increased, and indomethacin decreased LI significantly. In 6-day ulcer rats that were given ³H-thymidine only during the first day LI was 5%, while in those given ³H-thymidine only during the last day LI was 27%. LI and silver grain counting results indicated that during the first 6 days of healing the epithelial cells in the ulcer margin divide twice. In the undamaged epithelium of the 1-day ulcer rats LI was <one-third, and in the antral epithelium one-half of that in the non-ulcer controls. Conclusions. During the first 6 days of healing, the LI of the non-parietal epithelial cells increases exponentially in the ulcer margin; this is enhanced by gastrin. The unexpected finding in the ulcer rats of decreased LI in undamaged oxyntic and antral epithelium may be caused by a block of the G1 restriction point in the cell cycle. The reason for this remains obscure.

• Acetic ulcer
• antral mucosa
• gastrin
• indomethacin
• labeling index
• oxyntic mucosa
• rats