Gastric Acid Secretion in Gastric Fistula Cats before and after Vagotomy and in Vagotomized Gastric Fistula Cats during Reserpine Treatment1

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Abstract
In nonanesthetized cats with gastric fistulae reserpine ijencted daily for 3 days or more increased basal gastric secretion of acid and the acid secretory responses to intravenous histamine and gastrin. The increases had in an earlier study been shown to persist after symphathectomy and the main purpose of the present study was to determine the effect of vagotomy on these increases. Vagotomy significantly reduced the secretory responses of non‐anesthetized cats to histamine and gastrin and after vagotomy reserpine treatment did not produce any increase of basal secretion or of the secretory responses to histamine and gastrin. The latter finding proves that intact vagal innervation of the stomach is necessary for the development of hypersecretion during reserpine treatment. Maximal subthreshold amounts of methacholine infused intravenously into vagotomized cats produced increases of the secretory responses to histamine and gastrin approximately equal to those produced by reserpine treatment in cats before vagotomy. It is suggested that the reduction of the responses following vagotomy is due mainly to the elimination of the vagal tone which in the fasting cats is assumed to sensitize the parietal cells to histamine and gastrin. The hypersecretory effects of reserpine treatment in cats with gastric fistulae and the absence of these effects after vagotomy demonstrates that reserpine treatment increases the sensitivity of the parietal cells to histamine and gastrin only in the vagally innervated stomach. The increased sensitivity is supposed to be due to a centrally irduced enhancement of vagal tone. The increases in the secretory responses of vagotomized cats during the infusion of subthreshold amounts of methacholine are consistent with this explanation.