Abstract
G A A b st ra ct s was recorded at termination. Blood was collected for determination of serum gastrin. The histological changes in the stomachs were examined. The presence of dysplasia and carcinoma on the anterior and posterior side of the stomachs were compared, and the oxyntic mucosal thickness and neuroendocrine (chromogranin A positive) cell density were calculated. Results: Ten of fifteen animals operated by anterior vagotomy and 11 of 16 sham-operated developed hypergastrinemia. Vagotomy did not affect intragastric pH or serum gastrin. There was no difference between innervated and denervated oxyntic mucosa in dysplasia and carcinoma development. However, vagotomy resulted in lower stomach weight in hypergastrinemic animals (2.8 ± 0.26 g vs. 3.7 ± 0.39 g, p=0.027) and reduced oxyntic mucosal thickness on the anterior side (0.83 ± 0.06 mm vs. 1.13 ± 0.1 mm, p ,0.01). Vagotomy also resulted in a reduction in volume density of chromogranin A positive cells in the oxyntic mucosa (12.1 ± 1.8 % vs. 18.8 ± 3.0 %, p=0.04). Conclusions: Unilateral truncal vagotomy reduced the trophic effects of hypergastrinemia on the ECL cell and oxyntic mucosa, but did not prevent gastric carcinogenesis in female Japanese cotton rats. The effects of vagotomy on gastric carcinogenesis in animal models are conflicting and further studies in patients should be done to clarify the clinically significant effects of vagotomy.
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