gastrins and Esophageal-Fistula

To determine the role of endogenous pancreatic polypeptide (PP) as a physiological inhibitor of pancreatic secretion, normal rabbit serum (control) or rabbit PP-antiserum was administered intravenously to dogs with chronic esophageal, gastric, and pancreatic fistulas. In all dogs tested, sham-feeding and ordinary feed with a meat meal resulted in a marked rise in the plasma level of immunoreactive PP that coincided with an increase in the exocrine pancreatic secretion of HCO3- and protein. After intravenous administration of PP antiserum, endogenous plasma PP was almost completely bound by infused antibodies to PP, whereas no such binding was detected after infusion of normal rabbit serum. In contrast, plasma gastrin remained unchanged both under basal and stimulated conditions. Immunoneutralization of PP, released endogenously, failed significantly to affect gastric acid and pancreatic protein responses to sham-feeding and the pancreatic HCO3- and protein responses to feeding a meat meal in chronic pancreatic fistula dogs. However, the PP antiserum abolished, in part, the inhibitory effect of exogenous PP on pancreatic secretion stimulated by exogenous hormones. We conclude that endogenous PP is not a physiological inhibitor of exocrine pancreatic secretion, as has been suggested previously.

Topics: Animals; Antibodies; Bicarbonates; Dogs; Eating; Esophageal Fistula; Gastric Acid; Gastric Fistula; Gastrins; Islets of Langerhans; Pancreatic Fistula; Pancreatic Polypeptide; Proteins; Rabbits; Secretin; Sincalide

Canines with vagally innervated fundic pouches and chronic esophageal fistulas were subjected to sham feeding experiments during which pouch acid output and peripheral serum gastrin levels were measured. These dogs then underwent construction of vagally innervated antral pouches. The sham feeding experiments were repeated after recovery. Preoperatively sham feeding provoked a substantial increase in acid output accompanied by a small serum gastrin increase which did not achieve statistical significance. After creation of the innervated antral pouches, sham feeding evoked an acid secretory response similar to control values. Serum gastrins, however, increased nearly 500 percent in response to sham feeding. Our data support the concept that direct vagal stimulation of the parietal cell mass is the major mechanism by which sham feeding increased acid secretion.

Topics: Animals; Dogs; Esophageal Fistula; Food; Gastric Acidity Determination; Gastric Juice; Gastrins; Pyloric Antrum; Vagus Nerve

Dogs were provided with oesophageal fistulae, fully innervated pouches of the fundic stomach and the duodenal bulb, and a gastric cannula. Gastric secretion was stimulated by sham feeding for 10 min. The bulbar pouches were perfused either with 0.9 per cent NaCl or with 0.1 N HCl. Plasma gastrin concentrations were determined by radioimmunoassay. Bulbar acidification effectively inhibited gastric acid secretion. Plasma gastrin responses were not suppressed. Instead, plasma gastrin concentrations were higher than in controls. The results show that the bulbar mechanism does not inhibit gastric acid secretion by reducing gastrin release.

Topics: Animal Feed; Animals; Depression, Chemical; Dogs; Duodenum; Esophageal Fistula; Esophagus; Gastric Acidity Determination; Gastric Juice; Gastrins; Hydrochloric Acid; Perfusion; Secretory Rate; Sodium Chloride; Stimulation, Chemical; Stomach