A study of the literature is not at all convincing as to the effect of atropin on the stomach, especially its clinical effect on the human stomach. While on laboratory animals its effects seem to be quite definite, the reverse is true, according to the literature, when the drug is used in clinical medicine for the purpose of lessening spasm or reducing secretion.
Auer and Meltzer1 assert that atropin causes paralysis of the vagus endings connected with the ganglia of Auerbach's plexus and that the action is on the myoneural junction. Cushny2 states that the secretion of gastric juice has been shown to be diminished or entirely arrested by atropin, which paralyzes the termination of the secretory fibers of the vagus, and that the hydrochloric acid is more reduced than the pepsin or total fluid.
Zunz and Tysebaert3 found that in dogs, after a hypodermic of from 0.005 to 0.01