SHAM FEEDING AND PANCREATIC-SECRETION - EVIDENCE FOR DIRECT VAGAL-STIMULATION OF ENZYME OUTPUT

  • 1 January 1984
    • journal article
    • research article
    • Vol. 87  (1) , 109-114
Abstract
The cephalic phase of pancreatic secretion in humans was investigated using modified sham feeding and a duodenal perfusion system. Studies performed in 5 normal volunteers were designed so that trypsin and bicarbonate outputs during sham feeding, with or without pretreatment with atropine, were compared to maximal pancreatic secretory response to exogenous stimulation with caerulein and secretin. The role of gastric acid entry to the duodenum in mediating cephalic responses was assessed by a comparison between outputs observed when gastric aspiration (.simeq. 80% efficient) was used alone and when acid entry was completely abolished by combining gastric aspiration with cimetidine pretreatment. To evaluate the role, if any, of gut hormone release in the pancreatic secretory response to sham feeding, plasma gastrin and cholecystokinin [CCK] concentrations were monitored throughout. Trypsin outputs during sham feeding were 31.9 .+-. 10.45 kallikrein inactivator units [KIU]/30 min, equivalent to 4 times basal output and 92% of maximal, but were only 54% maximal in subjects pretreated with cimetidine. Atropine suppressed basal trypsin output and abolished the response to sham feeding (4.98 .+-. 3.89 KIU/30 min). A modest increase in bicarbonate secretion during sham feeding (3.30 .+-. 1.97 mmol/30 min vs. basal of 0.68 .+-. 0.74 mmol/30 min, P = 0.5) was not influenced by atropine but was abolished by cimetidine pretreatment. No significant changes in plasma gastrins were observed in these studies and plasma CCK remained undetectable throughout. There apparently is tonic vagal stimulation of trypsin secretion, and sham feeding markedly increases trypsin output, which is further augmented by acid entry into the duodenum. There is no direct effect of cephalic stimulation on bicarbonate secretion or on gastric or CCK release.