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Epithelial restitution and cellular proliferation after gastric mucosal damage caused by hypertonic NaCl in rats

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Summary

Hypertonic NaCl enhances gastric cancer in rats induced by N-nitroso compounds. This study was designed to examine the structural changes and alterations in mitotic activity occurring after mucosal exposure to hypertonic NaCl. Wistar rats were given one ml of 4.5 M NaCl by gastric tube and groups of 4–5 animals were sacrificed at different time intervals up to 120 h. An i.p. injection of thymidine was given 1 h before death. Samples of antral and corpus mucosa were prepared for microscopy and autoradiography. Hypertonic NaCl caused uniform destruction of surface mucous cells and pits in the corpus and antrum. Epithelial restitution with the formation of a thin epithelial layer occurred within one h of damage. The mucosa changed towards normal within 24–48 h. The distance between mucosal surface and the replicating cells decreased during the first 2 h. The proliferation zone remained in the middle of the glandular layer throughout the experiment. The proliferative activity increased during the first 24 h after mucosal damage. The number of labelled cells per unit area of mucosa was somewhat larger in the corpus than the antrum, but in the corpus the distance between proliferating cells and mucosal surface was double that of the antrum. Hypertonic NaCl causes a series of changes in the gastric mucosa. The increased mitotic activity can only partly explain the cocarcinogenic effect, since N-nitroso-induced adenocarcinomas occur predominantly in the antrum while the mitotic activity is maximal in the corpus.

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This work was supported by the Norwegian Cancer Society, the Norwegian Council for Science and the Humanities, and Helga Sembs Fond

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Sørbye, H., Svanes, C., Stangeland, L. et al. Epithelial restitution and cellular proliferation after gastric mucosal damage caused by hypertonic NaCl in rats. Vichows Archiv A Pathol Anat 413, 445–455 (1988). https://doi.org/10.1007/BF00716993

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  • DOI: https://doi.org/10.1007/BF00716993

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