The effects of fundic
vagotomy on
acid and
pepsin secretion in 12 patients (10 males, two females; nine
duodenal ulcer, three
gastric ulcer) were studied using a
pentagastrin dose response before and after
Vagotomy. In the intact stage H, Cl, and
pepsin output all had the same ED50, 120-127 pmol/kg/h.
Vagotomy reduced basal output of
acid by 78%, Cl- by 50%, and
pepsin by 62%. Postvagotomy basal outputs were not related to preoperative levels, while maximum
acid output was reduced by an average of 35%, proportionally to the preoperative output (r = 0.94).
Vagotomy uncompetitively (ED50 increase, Vmax decrease) inhibited the
pentagastrin dose response of
acid,
chloride, and
pepsin output. Postoperatively, a six-fold greater dose of
pentagastrin (450 vs 76 pmol/kg/h) was required to stimulate
acid to 50% of its preoperative maximum output. For
pepsin secretion the increase was 12-fold (185 vs 15 pmol/kg/h). In five of the nine
duodenal ulcer patients
pentagastrin dose responses were repeated with a background infusion of
urecholine, 20 micrograms/kg/h.
Urecholine increased basal and peak
acid,
pepsin, and
chloride outputs, and the ratio of basal: maximal almost to prevagotomy levels; it also restored the sensitivity to
pentagastrin. Serum
gastrin was not significantly changed by
urecholine or by
vagotomy. We conclude that the level of basal
acid and
pepsin secretion in
ulcer patients, which is largely eliminated by
vagotomy, is dependent on the vagus and not on serum
gastrin. The effects of
vagotomy are functional, are due to
cholinergic withdrawal, and usually can be restored by
cholinergic replacement.