The role of sympathetic innervation and sympathomimetics in gastric secretion in vivo.

It can, I believe, be argued in summary that pentagastrin-stimulated acid and pepsin secretion from innervated or denervated fundic mucosa is inhibited by doses of epinephrine and isoproterenol that produce an unequivocal cardiac stimulation, but this cannot be said of either histamine-, bethanechol-, or methacholine-, or food-stimulated secretion. There is substantial old evidence that epinephrine and isoproterenol, in doses that depress the pentagastrin effect, actually augment that of histamine and cholinomimetics. Large doses, of course, inhibit unequivocally. Sympathectomy, chemical or surgical, seems to increase the responsiveness of the fundus to acid stimuli, but again there is little uniformity; both less acid following feeding, after sympathectomy, and more following propranolol have been reported. It would be rash to draw any conclusions from the action of either sympathetic stimulation or ablation. The evidence that beta-adrenergic blocking agents can prevent insulin-stimulated increases in gastrin is fairly good, but the evidence that these agents have any effect on food-stimulated gastrin levels (whether the food is a meal or sham) is not good. Almost every aspect of this subject remains confused and confusing. At the end of a paper such as this, most readers would expect conclusions, but any conclusions other than those given above would be invention or else bias. This subject, at present unfashionable for research, represents a black hole in our knowledge.(ABSTRACT TRUNCATED AT 250 WORDS)