The basal and food-stimulated gastrin secretion after selective proximal vagotomy, selective gastric vagotomy and truncular vagotomy was found to be elevated. Hypergastrinemia increased as gastric secretion was inhibited, thus attesting to the role of acid formation inhibition in the origin of the postvagotomy increase in the hormonal secretion. However the values of the intragastral pH being equal, the blood gastrin level was higher after vagotomy as compared to that seen in unoperated peptic ulcer patients. After vagotomy coupled with antrumectomy gastrin secretion remained at the level seen in the unoperated patients, indirect evidence for increased function of extraantral G cells. Inhibition of gastric secretion is no single cause of the postvagotomy hypergastrinemia, since the latter was essentially increased in the early postoperative times and in the presence of the vagotomy-induced disorders. It is concluded that increased secretion of gastrin after vagotomy secures trophic and compensatory-adaptation processes.
Adult Duodenal Ulcer