Parietal cell density during gastric ulcer healing in the rat

During the healing of gastric ulcers, extensive changes take place in the structure and proportion of the parietal cells in the ulcer margin. We aimed to determine whether these changes are influenced by compounds or by procedures that may promote or delay gastric ulcer healing.

Acetic acid ulcers were produced in the rat gastric corpus; control rats were non-operated or sham-operated. All rats were provided with an osmotic minipump releasing 3H-thymidine for determination of the labelling index (LI). The rats were given omeprazole, gastrin or indomethacin, infected with Helicobacter pylori, or subjected to anterior vagotomy. They were killed after 1, 2, 6 or 13 days, and the ulcer margin and undamaged corpus wall were excised for histology. The proportion of parietal cells was calculated in relation to the total number, and the total volume, of the epithelial cells.

The parietal cells averaged 16%-21% of the number and 30%-32% of the volume of the epithelial cells in the unoperated control rats, but considerably less in the ulcer margin. This reduction was partially prevented by indomethacin. In the undamaged, dorsal epithelium the parietal cells increased to 23%-26% of the number, and 41%-47% of the volume, of the epithelial cells, both in the ulcer rats and in the sham-operated rats. The LI of the parietal cells was 6% in the undamaged epithelium of the 13-day ulcer rats, but close to 0% in all other groups examined.

Indomethacin prevents much of the loss of parietal cells in the ulcer margin. In the undamaged epithelium of the ulcer rats there is an increased proportion of parietal cells. The new parietal cells are not formed directly from dividing cells, but are probably recruited from existing precursor cells.