The reason for increased maximal acid secretory capacity in some patients with duodenal ulcer is uncertain. We postulated that chronically increased cephalic-vagal stimulation may be a cause of increased maximal acid output. To study this, we prepared six male, mongrel dogs with a vagally innervated gastric fistula, a vagally denervated fundic (Heidenhain) pouch, and a cervical esophagostomy. Physiological cephalic-vagal stimulation was accomplished by sham feeding, which increased acid output from the vagally innervated stomach but not from the vagally denervated pouch. During an initial 6-wk control period, dogs were fed by mouth once daily at 3 p.m. Then, a 6-wk period of sham feeding was carried out, during which animals were sham fed with blenderized dog chow from 8 a.m. to 3 p.m. every day (a 7-h period of continuous cephalic-vagal stimulation), after which animals were fed by mouth. After 6 wk of daily sham feeding, maximal acid output in response to intravenous pentagastrin (16 micrograms/kg per h) increased by 27 +/- 4% in the vagally innervated stomach (P less than 0.01). Maximal acid output then returned to control levels after a final 6-wk recovery period with no sham feeding. No changes in maximal acid output occurred in the vagally denervated pouch during the 18-wk study. No changes in basal acid secretion or responsiveness of parietal cells to submaximal doses of pentagastrin occurred in the fistula or pouch during chronic sham feeding. We conclude that chronic physiological cephalic-vagal stimulation can increase maximal acid secretory capacity. Our studies also suggest that the effect of chronically increased vagal stimulation on maximal acid secretory capacity is reversible.
R C Thirlby, M Feldman