Promotion by vagotomy of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.
The effects of truncal vagotomy after administration of N-methyl-N'-nitro-N-nitrosoguanidine on the incidence and number of gastric carcinomas and gastric acid secretion, gastrin secretion, antral pH, and duodenal reflux were investigated in inbred Wistar rats. Rats were subjected to truncal vagotomy after N-methyl-N'-nitro-N-nitrosoguanidine treatment. Vagotomy significantly increased the incidence and number of adenocarcinomas of the glandular stomach. It also resulted in significantly more atypical glandular hyperplasias, which are precursors of gastric cancer. Furthermore, it caused a decrease in gastric secretion and an increase in mucosal pH in the antrum but did not increase duodenal reflux. These findings indicate that vagotomy has a promoting effect on the development of gastric cancers. The reduced gastric acid secretion, but not duodenal reflux, may be related to this increased incidence of gastric cancer.
D000818:Animals; D001835:Body Weight / Q000187:drug effects; D004383:Duodenogastric Reflux / Q000503:physiopathology; D005744:Gastric Acid / Q000378:metabolism; D005750:Gastric Juice / Q000187:drug effects; D005755:Gastrins / Q000378:metabolism; D008297:Male; D008769:Methylnitronitrosoguanidine / Q000633:toxicity; D051381:Rats; D011919:Rats, Inbred Strains; D013274:Stomach Neoplasms / Q000139:chemically induced / Q000473:pathology*; D013997:Time Factors; D014628:Vagotomy
D005755:Gastrins; D008769:Methylnitronitrosoguanidine