We studied post-meal pancreatic secretion and gastrin release in conscious dogs with duodenal Thomas cannulas. Normal dogs were tested in physiological conditions and with an i.v. infusion of atropine 20 pglkglh or secretin 0.5 CU/kg/h. The responses were also studied after antral and truncal vagotomy. In the early phase (0-20 min) of the response, before gastric emptying started, antral vagotomy reduced fluid and protein outputs, and truncal vagotomy reduced them still more. Atropine reduced only the protein response. Gastrin release reached a peak after 2&25 min. After antral and truncal vagotomy, gastrin release was reduced within 10 min after the meal. Latephase (>20 min) pancreatic secretion depended on the presence of chyme in the duodenum. The effects of atropine and antral vagotomy in the cephalogastric phase could be explained by antropancreatic reflexes stimulating fluid secretion (atropine-resistant pathway) and protein output (atropine-sensitive pathway).
Serum gastrin and pancreatic secretion were measured in conscious Thomas fistula dogs during infusion of increasing doses of porcine gastrin, against a background of secretin. Dose-response relationships were calculated for the effects of gastrin on pancreatic secretion. Gastrin release was also measured after a test meal and after vagal stimulation with 2-deoxyglucose. Peak serum gastrin levels after these stimuli were less than the serum gastrin level associated with the minimal effective dose of gastrin. From the dose-response relationship of serum gastrin and pancreatic protein output, it was possible to calculate the protein output corresponding to the peak gastrin levels after 2-deoxyglucose or a meal. These were equivalent to 20-30% of the observed protein response to these stimuli. We conclude that gastrin plays at most a small part in the stimulation of pancreatic secretion after a meal and in response to 2-deoxyglucose. We also found that truncal vagotomy reduces pancreatic sensitivity to gastrin. Key Words: Pancreas secretion-GastrinTest meal-Vagotomy -2-Deoxyglucose.Gregory and Tracy (1) were the first to isolate gastrin. They demonstrated that gastrin could stimulate pancreatic secretion, mostly of protein. Since then the assumption has been made that gastrin acts in this way under physiological conditions. The same stimuli (e.g., insulin hypoglycemia or sham feeding) both increase serum gastrin (2,3) and stimulate pancreatic secretion (4,5), but no comparison has been made between serum levels of gastrin obtained with these simulants and the levels necessary to stimulate the pancreas. The finding that selective total gastric vagotomy (SGV) or antrectomy (either total or mucosal) reduces pancreatic response to metabolic vagal stimulation with 2-deoxyglucose or insulin by about 75% (5,6) was interpreted to mean that vagally mediated gastrin release played a large part in the control of pancreatic secretion.On the other hand, it seems unlikely that gastrin is a physiological stimulant of pancreatic secretion in view of the much lower potency of gastrin than cholecystokinin, which acts on the same receptors (7). In addition, it has been shown, firstly that exogenous gastrin can restore only half of the lost secretion after removal of the antral mucosa (8), and secondly that gastropancreatic reflexes are more likely than gastrin to be involved in at least some pancreatic responses. For example, distension of an antral pouch causes a rise in pancreatic secretion: this response is abolished by atropine and reduced by 90% after truncal vagotomy (9). Therefore, it likely that the pancreatic response to antral distension is mediated largelv bv neural re-
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