Colonic carcinogenesis in vagotomyzed rats

An increased incidence of colorectal cancer (CRC) has been reported in patients with peptic ulcer disease treated with truncal vagotomy. Inhibition of gastric acid output and its hormonal consequence, hypergastrinemia, have been considered risk factors for the development of CRC. The aim of the present study was to determine whether truncal vagotomy increases, in the short (7 days) and long term (120 days), the incidence of CRC in a model of carcinogenesis.

We used 86 Wistar rats distributed in 7 groups to which DMH (1,2-dimethylhydrazine dihydrochloride) was administered for the induction of colon tumors, at doses of 5 and 20 mg/kg of weight. The first three groups were used as control groups; the rats of the four other groups underwent a truncal vagotomy with pyloroplasty and Heller myotomy prior to the administration of DMH. Finally, we compared the incidence of colonic tumors in vagotomized vs non-vagotomized groups receiving the same dose of DMH.

In the non-vagotomized rats that received low doses of DMH (5 mg/kg of weight), mortality was 0% and 0% developed cancer as compared to 40% and 0%, respectively, of rats vagotomized 7 days before the administration of DMH and 20% and 0%, respectively, of rats vagotomized 120 days before the administration of DMH. After the administration of high doses of DMH, mortality was 50% and 80% developed cancer as compared to 100% and 0%, respectively, of rats vagotomized 7 days before the administration of DMH and 61.11% and 42.8%, respectively, of rats vagotomized 120 days before the administration of DMH.

Truncal vagotomy does not increase the incidence of CRC induced by DMH in the rat.