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Secretin and cholecystokinin (CCK-PZ) were administered intravenously in graded doses to live anesthetized dogs. Pancreatic secretion and tissue biopsies were analyzed for cyclic AMP content. Both secretin and CCK-PZ caused an output of cyclic AMP into pancreatic secretion, secretin being a more potent stimulant than CCK-PZ. The concentration of cyclic AMP in the pancreatic juice increased with increasing doses of secretin but not with CCK-PZ. Tissue cyclic AMP content remained unchanged during infusion of either secretin or CCK-PZ. Infusion of aminophylline with secretin did not potentiate the action of secretin. It is concluded that synthesis of cyclic AMP in the dog pancreas is stimulated by both secretin and CCK-PZ and that the newly synthesized cyclic AMP is rapidly secreted into pancreatic juice, resulting in a steady content of tissue cyclic AMP.

Four mongrel dogs were prepared with a Heidenhain pouch, a gastric fistula, and a 90-cm-long Thiry-Vella loop. After recovery, dose-response curves were obtained with different doses of pentagastrin, and the maximal acid output was determined. The jejunal loop was perfused for 3 h with either 5% liver extract or with 0.15 M NaCl at a rate of 114 ml/h. To verify that the stomach could release gastrin and that the assay could detect that change, antral perfusion with liver extract was performed. Serum gastrin levels and acid output were measured every 30 min. Perfusion of the jejunal loop with liver extract resulted in a significant increase in acid output from the Heidenhain pouch and the gastric fistula, whereas perfusion with saline solution failed to show any changes. The magnitude of acid response from the Heidenhain pouch and gastric fistula was 11% and 18%, respectively, as compared with maximal pentagastrin stimulation. The serum gastrin levels remained unchanged during both liver extract and saline perfusion of the jejunal loop, in contrast to the marked increase in serum gastrin level after antral perfusion. The results confirm the existence of the intestinal phase of gastric acid stimulation in dogs as an entity and show that the magnitude of this phase is significantly lower than has been suggested by results of earlier studies. Furthermore, the results suggest that the intestinal phase of gastric secretion in dogs is most probably elicited through a humoral agent other than gastrin.

The rate of protein phosphorylation, as catalyzed by the protein kinase enzymes, was measured in the pancreas of rats with acute experimental pancreatitis. Two different methods were used to induce pancreatitis in rats: retrograde injection of deoxycholate (DOC) into the pancreatic duct, or daily intravenous administration of DL-ethionine. Basal protein kinase activity was elevated in rats with acute experimental pancreatitis. This increase in activity was not dependent on free Ca2+ and did not result from elevated cAMP levels. To assess the possible role of digestive enzymes in protein kinase activation, tissue extracts from healthy controls were subjected to mild treatment with digestive enzymes and DOC. Trypsin, chymotrypsin, phospholipase A, and DOC produced protein kinase activation of a similar magnitude as found in diseased tissue. Results indicate that stimulated protein kinase activity in tissue of animals with acute pancreatitis may arise from the action of digestive enzymes.

Vagotomy is a dynamic, evolving therapeutic tool rather than the “simple” operation it is sometimes assumed to be. Postoperative ulcer recurrence remains a problem, and the development of a foolproof peroperative test for completeness of vagotomy will be welcome.

There is a definite need for surgeons with an interest in gastrointestinal problems to develop and maintain expertise in gut endoscopy. In this article we emphasize the interpretation of symptoms in postoperative patients as a focal point, although other illustrations might be cited. While stressing the role of surgeons in this respect, it is essential to underscore the complementary roles of surgeons and physicians, and to emphasize that both disciplines' points of view are needed to determine the source of patients' complaints. The special awareness that a surgeon brings to the analysis of these postoperative problems results from a knowledge of postoperative patients in general, supplemented by an awareness of technical factors that might either influence the operation's success or explain a new symptom occurring in the postoperative period.