cholecystokinin and Pancreatic-Fistula

There have been no previous reports whether long-term bile diversion enhances pancreatic exocrine secretion. The aim of this study was to elucidate the effect of long-term bile diversion on pancreatic exocrine secretion. Four mongrel dogs were prepared for chronic gastric and pancreatic fistulas and received intraduodenal sodium oleate infusion (controls). These dogs, then underwent diversion of bile from the intestines by ligating the common bile duct and interposing a segment of jejunum between the gallbladder and the urinary bladder (total biliary diversion [TBD]). After three weeks, the dogs received an identical sodium oleate infusion. TBD augmented basal pancreatic exocrine secretion compared with controls (4.4-fold increase in basal flow volume; 9.0-fold increase in bicarbonate output; and 3.3-fold increase in protein output). Likewise, TBD augmented oleate-stimulated exocrine secretion (2.0-fold increase in cumulative flow volume; 2.6-fold increase in bicarbonate output; and 1.4-fold increase in protein output). TBD also augmented basal and oleate-stimulated plasma cholecystokinin levels. Administration of a Cholecystokinin-A receptor antagonist (loxiglumide) after TBD reduced the flow volume and bicarbonate output to the control levels, and the protein output to less than a half of the control level. Long-term bile diversion enhances basal and oleate-stimulated pancreatic exocrine secretion, at least partly via increased cholecystokinin secretion.

Topics: Animals; Bicarbonates; Bile Ducts; Cholecystokinin; Dogs; Duodenum; Gastric Fistula; Hormone Antagonists; Humans; Oleic Acid; Pancreas; Pancreatic Fistula; Proglumide; Receptor, Cholecystokinin A; Time Factors; Urinary Bladder

The mechanism behind the possible feedback regulation of pancreatic exocrine secretion is not well understood.. Thirteen minipigs were prepared with fistulas to the pancreatic duct and the duodenum. Peripheral venous blood was obtained for determination of secretin and cholecystokinin (CCK) levels. Four different experiments were performed: 1) diversion and reinfusion of pancreatic juice; 2) intraduodenal infusion of NaHCO3 solution, with the same volume, bicarbonate concentration, and osmolality as the collected pancreatic secretion, and reinfusion of pancreatic juice; 3) reinfusion of pancreatic secretion for 1 h before and 2 h after a meal; and 4) diversion of pancreatic secretion and intraduodenal infusion of NaHCO33 solutions before and after a meal.. Reinfusing pancreatic juice significantly decreased pancreatic juice volume and bicarbonate output and slightly decreased the level of secretin in plasma. Alternating infusions of substitute NaHCO3 and pancreatic juice did not change pancreatic output of bicarbonate and protein, nor did it change the CCK and secretin levels in plasma. Replacing pancreatic juice with intraduodenal NaHCO3 infusions during a meal did not significantly modify the pancreatic secretion of bicarbonate and protein or the hormonal levels in blood.. A negative feedback regulation of pancreatic exocrine secretion is present in starved minipigs. Duodenal acidity and plasma levels of secretin semm to be of importance, whereas duodenal enzyme activity and the level of CCK in plasma probably are not. A postprandial negative feedback regulation through duodenal enzymatic activity and release of CCK into blood could not be shown.

Topics: Animals; Cholecystokinin; Duodenal Diseases; Feedback; Food; Intestinal Fistula; Pancreas; Pancreatic Fistula; Pancreatic Juice; Secretin; Sodium Bicarbonate; Starvation; Swine; Swine, Miniature

Although previous reports suggest interactions between the endocrine and the exocrine pancreas, insulin's effect on pancreatic exocrine function remains unclear. Chronic pancreatic fistulae were created in five dogs; these animals were studied using the euglycemic, hyperinsulinemic clamp technique. After a 30-min unstimulated period, both groups received a 60-min, 1.5 mU/kg/min insulin (clamp) or vehicle (control) infusion. Cholecystokinin (CCK) or meal stimulation was then begun. Intravenous CCK was initiated at 12.5 ng/kg/h; the CCK dose was doubled every 30 min until 100 ng/kg/h was achieved. The intraduodenal liquid test meal (1.5 kcal/ml; 15% protein, 32% fat, 53% carbohydrate) was administered at 100 ml/h. Unstimulated (0- to 30-min) serum glucose and insulin levels and pancreatic bicarbonate and protein outputs did not differ between groups. Clamp (30- to 90-min) and stimulated (90- to 210-min) insulins were significantly elevated in clamp groups (p < 0.001); glucose and bicarbonate were unchanged. Exocrine outputs during clamp periods were unaffected by insulin. Neither CCK- nor meal-stimulated pancreatic secretion (90-210 min) was influenced by insulin administration. These data suggest that hyperinsulinemia does not alter pancreatic acinar cell secretion in the intact animal.

Topics: Animals; Bicarbonates; Blood Glucose; Cholecystokinin; Dogs; Food; Glucose Clamp Technique; Insulin; Pancreas; Pancreatic Fistula; Proteins

This study was designed to determine the role of cholecystokinin (CCK) in the inhibition of gastric HCl secretion by duodenal peptone, fat and acid in dogs with chronic gastric and pancreatic fistulas. Intraduodenal instillation of 5% peptone stimulated both gastric HCl secretion and pancreatic protein secretion and caused significant increments in plasma gastrin and CCK levels. L-364,718, a selective antagonist of CCK-A receptors, caused further increase in gastric HCl and plasma gastrin responses to duodenal peptone but reduced the pancreatic protein outputs in these tests by about 75%. L-365,260, an antagonist of type B receptors, reduced gastric acid by about 25% but failed to influence pancreatic response to duodenal peptone. Addition of 10% oleate or acidification of peptone to pH 3.0 profoundly inhibited acid secretion while significantly increasing the pancreatic protein secretion and plasma CCK levels. Administration of L-364,718 reversed the fall in gastric HCl secretion and significantly attenuated pancreatic protein secretion in tests with both peptone plus oleate and peptone plus acid. Exogenous CCK infused i.v. in a dose (25 pmol/kg per h) that raised plasma CCK to the level similar to that achieved by peptone meal plus fat resulted in similar inhibition of gastric acid response to that attained with fat and this effect was completely abolished by the pretreatment with L-364,718. We conclude that CCK released by intestinal peptone meal, containing fat or acid, exerts a tonic inhibitory influence on gastric acid secretion and gastrin release through the CCK-A receptors.

Topics: Animals; Benzodiazepinones; Bethanechol Compounds; Cholecystokinin; Devazepide; Dogs; Gastric Acid; Gastric Fistula; Gastrins; Histamine; Hydrogen-Ion Concentration; Oleic Acid; Oleic Acids; Pancreatic Fistula; Peptones; Phenylurea Compounds; Receptors, Cholecystokinin; Sincalide

Pancreatic secretion in rats is regulated by feedback inhibition of cholecystokinin (CCK) release by proteases in the gut lumen, but little is known about the role of gastric acid in this regulation. This study, carried out on conscious rats with large gastric fistulas (GF) and pancreatic fistulas, shows that diversion of pancreatic juice results in the progressive stimulation of pancreatic secretion only in rats with the GF closed. When the GF was kept open, the diversion resulted in only small increment in pancreatic secretion and this was accompanied by progressive increase in gastric acid outputs. Similar amounts of HCl instilled into the duodenum in rats with the GF open fully reproduced the increase in pancreatic secretion observed after the diversion of pancreatic juice. Pretreatment with omeprazole (15 mumol/kg) to suppress gastric acid secretion or with L-364,718 (5 mumol/kg) to antagonize CCK receptors in the diverted state, resulted in the decline in pancreatic secretion similar to that observed after opening the GF. CCK given s.c. (20-320 pmol/kg) failed to cause any significant rise in the post-diversion pancreatic secretion in rats with the GF closed, but stimulated this secretion dose-dependently when the GF was open. Camostate (6-200 mg/kg) in rats with pancreatic juice returned to the duodenum caused dose-dependent increase in pancreatic secretion, but after opening the GF or after omeprazole this increase was reduced by about 75%. This study provides evidence that gastric acid plays a crucial role in the pancreatic response to diversion of pancreatic juice or inhibition of luminal proteases, and that factors that eliminate gastric acid secretion reduce this response.

Topics: Animals; Benzodiazepinones; Cholecystokinin; Devazepide; Esters; Feedback; Gabexate; Gastric Acid; Gastric Fistula; Guanidines; Male; Omeprazole; Pancreas; Pancreatic Fistula; Protease Inhibitors; Rats; Rats, Wistar

Exocrine pancreatic response to food is believed to result from the interaction of neural and hormonal factors, but their contribution in the net postprandial secretion is unknown. Recent description of a highly specific and potent cholecystokinin (CCK)-receptor antagonist permitted the evaluation of the physiologic role of CCK in postprandial pancreatic secretion. In dogs with chronic pancreatic fistula, CCK antagonism caused little alteration in sham feeding- or urecholine-induced pancreatic protein secretion, but reduced by approximately 60% the pancreatic protein response to a gastrointestinal meal and virtually abolished the pancreatic responses to duodenal perfusion with amino acids or oleate and to exogenous CCK, but not to secretin or neurotensin. The pancreatic protein responses, particularly to lower doses of gastrin, were also reduced by CCK-receptor antagonist, but no changes in the responses to secretin or neurotensin were detected. Cholecystokinin antagonism also significantly reduced the pancreatic polypeptide responses to CCK, gastrin, and the gastrointestinal meal, possibly due to removal of the CCK-mediated release of pancreatic polypeptide. We conclude that CCK plays a crucial role in the mediation of the gastrointestinal phase, but not the cephalic phase, of pancreatic secretion.

Topics: Animals; Cholecystokinin; Dogs; Food; Gastric Fistula; Gastrins; Glutamine; Pancreas; Pancreatic Fistula; Pancreatic Polypeptide; Proglumide; Receptors, Cholecystokinin

The objective of these studies was to investigate the role of bile salts in the regulation of release of cholecystokinin in response to nutrients in dogs and humans. In dogs, the intraduodenal administration of a bile salt sequestrant, cholestyramine (2, 4, or 8 g/h), resulted in a dose-related enhancement of the release of cholecystokinin-33/39 and pancreatic protein secretion in response to intraduodenal administration of amino acids. Intraduodenal administration of cholestyramine alone did not affect basal levels of cholecystokinin-33/39 or pancreatic protein secretion. Total diversion of bile also significantly increased the release of cholecystokinin and pancreatic protein secretion in response to intraduodenal administration of amino acids. Replacement of the bile salt pool by intraduodenal administration of taurocholate completely reversed the enhancement effect of both cholestyramine and bile diversion. In humans, oral ingestion of cholestyramine (12 g) significantly increased the release of cholecystokinin-33/39 and gallbladder contraction in response to the oral ingestion of either a triglyceride or amino acids. These results support a physiologic role of bile salts in the negative feedback regulation of release of cholecystokinin in response to luminal nutrients.

Topics: Adult; Animals; Bile Acids and Salts; Biliary Fistula; Cholecystokinin; Cholestyramine Resin; Dogs; Feedback; Female; Food; Gallbladder; Humans; Male; Pancreas; Pancreatic Fistula; Peptide Fragments

In dogs prepared with either pancreatic duct ligation (PDL) or chronic pancreatic fistula (PF), we investigated the effect of pancreatic enzymes on release of cholecystokinin (CCK) in response to corn oil in the upper small intestine. In control dogs without PDL, intraduodenal administration of corn oil (Lipomul containing 15 mmol of triglyceride) resulted in a marked and sharp increase in plasma CCK concentration during the 1st h, which then decreased during the following 1.5 h. In PDL dogs, on the other hand, no immediate increase occurred during the 1st 45 min after which a modest but gradual increase occurred in plasma CCK concentration during the following 2 h. Likewise, plasma CCK concentration increased significantly when Lipomul predigested with pancreatic enzymes or oleic acid was administered to PDL dogs. The increase was comparable to the response to Lipomul alone in control dogs. The infusion of Lipomul resulted in similar responses of plasma CCK in PF dogs as were found in PDL dogs when pancreatic juice was diverted to the exterior from the duodenum. The increases in plasma CCK paralleled the pancreatic protein secretion, and a significant correlation was found between plasma CCK concentration and the protein output. The present observations indicate that release of endogenous CCK by fat from the upper small intestine depends on an adequate digestion of neutral fat by pancreatic enzymes. Thus pancreatic enzymes play an important role on release of CCK in response to a neutral fat.

Topics: Animals; Cholecystokinin; Corn Oil; Dogs; Female; Intestine, Small; Ligation; Lipase; Male; Oleic Acids; Pancreas; Pancreatic Ducts; Pancreatic Fistula; Pancreatic Juice; Plant Oils

In dogs with pancreatic fistulas, meat feeding and intestinal perfusion with a sodium oleate or amino acid mixture increased pancreatic protein secretion to approximately 110, 100, and 50%, respectively, of the response to cholecystokinin (CCK) at a dose of 85 pmol X kg-1 X h-1. Plasma CCK response increased in these studies to approximately 100, 180, and 40%, respectively, of the value obtained with exogenous CCK, suggesting that, in addition to CCK, other neurohormonal factors contribute to pancreatic enzyme secretion in response to endogenous stimulants. Feeding and duodenal oleate or amino acids also stimulate the release of pancreatic polypeptide (PP), which may be involved in the control of pancreatic secretion in response to endogenous stimulants, including CCK. Perfusion of the intact intestine with graded amounts of oleate (0.5-16 mmol/h) produced dose-dependent increments in plasma CCK and pancreatic protein similar to those obtained with intravenous infusion of graded doses of CCK (0.85-255 pmol X kg-1 X h-1). Oleate perfusion of isolated Thiry loops (30 cm long) made of duodenojejunal (D-J) and ileal (I) segments also stimulated protein secretion but elevated plasma CCK only after perfusion of the D-J but not of the I loop. We conclude that 1) the endogenous CCK released by various luminal stimulants drives the pancreatic protein secretion; 2) the release of CCK is confined to the foregut; and 3) PP concomitantly released by various intestinal stimulants may contribute to the control of pancreatic secretion induced by endogenous CCK.

Topics: Animals; Atropine; Cholecystokinin; Dogs; Food; Gastric Fistula; Meat; Oleic Acid; Oleic Acids; Pancreatic Fistula; Pancreatic Polypeptide; Perfusion; Sincalide; Somatostatin

Truncal vagotomy results in diminished pancreatic protein secretion in response to intraduodenal fat. This diminished secretion may be due, at least in part, to interruption of the vagal reflexes between the intestine and the pancreas that work independently of cholecystokinin (CCK). In five dogs with chronic pancreatic fistulas, plasma CCK concentrations and pancreatic protein secretion in response to an intestinal stimulant (intraduodenal oleate) and to two exogenous peptides (bombesin and CCK-33) were compared before and after bilateral truncal vagotomy. Vagotomy decreased integrated protein secretion by about 50% in response to intraduodenal oleate. In contrast, protein output in response to parenteral stimuli increased after vagotomy. Integrated output of CCK in response to intraduodenal oleate or to exogenous bombesin or CCK was not significantly affected by vagotomy, but release of pancreatic polypeptide was decreased significantly in response to all stimuli after truncal vagotomy. These data provide evidence that truncal vagotomy decreases pancreatic protein secretion in response to intestinal stimulants by interrupting enteropancreatic reflexes mediated by the vagus, while maintaining normal (or supranormal) sensitivity of the pancreas to endogenous and exogenous CCK.

Topics: Animals; Bombesin; Cholecystokinin; Dogs; Duodenum; Female; Male; Oleic Acid; Oleic Acids; Pancreas; Pancreatic Fistula; Pancreatic Polypeptide; Peptide Fragments; Proteins; Reflex; Sincalide; Stimulation, Chemical; Vagotomy; Vagus Nerve

Topics: Animals; Cholecystokinin; Consciousness; Dogs; Dose-Response Relationship, Drug; Gastric Fistula; Gastrin-Releasing Peptide; Pancreas; Pancreatic Fistula; Pancreatic Juice; Pancreatic Polypeptide; Peptides; Stimulation, Chemical

The effects of loperamide on exocrine pancreatic secretion were studied in rats fitted with chronic or acute fistulas. Intraduodenal injection of loperamide in conscious rats resulted in a dose-dependent inhibition of basal pancreatic secretion involving volume and bicarbonate and protein output with an ED50 of about 0.5 mg/kg. The maximal inhibition observed was about 60% for volume and bicarbonate output and 90% for protein output. Loperamide induced an inhibition of pancreatic secretion in conscious rats that was naloxone-sensitive and persisted in cimetidine-treated rats. Thus, it did not depend on modifications of gastric secretion. In anaesthetized rats, loperamide did not inhibit the pancreatic secretion evoked by agents acting directly on the pancreatic cells (acetylcholine, secretin, CCK) but it inhibited by 100% the pancreatic secretion induced by vagal electrical stimulation (VES) and by 80-100% that induced by 5 thio-glucose, a centrally acting vagal stimulatory agent. Loperamide inhibition of VES-induced pancreatic secretion was different from that obtained with morphine or methadone since these opiate drugs could only inhibit by 50-60% maximally the VES-stimulated pancreatic secretion. The loperamide inhibition of VES-induced secretion was naloxone-insensitive, while loperamide inhibition of 5 thio-glucose-induced secretion was in part naloxone-sensitive. These results suggest that loperamide exerts a potent inhibition of pancreatic secretion by acting on the nerve supply to the pancreas through both opiate and non-opiate mechanisms.

Topics: Acetylcholine; Anesthesia; Animals; Bicarbonates; Cholecystokinin; Electric Stimulation; Glucose; Loperamide; Male; Naloxone; Pancreas; Pancreatic Fistula; Piperidines; Proteins; Rats; Rats, Inbred Strains; Vagus Nerve

We compared the inhibition of food-stimulated gastric acid secretion and changes in serum concentrations of immunoreactive gastric inhibitory polypeptide and gastrin caused by: (a) duodenal perfusion of oleic acid, and (b) intravenous infusion of pure, natural, porcine gastric inhibitory, polypeptide in dogs with gastric fistula and pancreatic fistula. A rate of duodenal perfusion of oleic acid (12 ml/hr) which gave near maximal pancreatic protein response was chosen. This dose of oleic acid caused complete suppression of acid response to a meal of liver extract (300 ml of a 15% solution) while elevating serum immunoreactive gastric inhibitory polypeptide modestly. By contrast, intravenous administration of gastric inhibitory polypeptide that raised serum immunoreactive gastric inhibitory polypeptide several fold caused only 40% inhibition of acid response to the same meal. Other effects of duodenal perfusion of oleic acid were exaggeration of pancreatic protein secretion and significant inhibition of gastrin release in response to the meal. Exogenous administration of gastric inhibitory polypeptide, on the other hand, was without significant effect on these responses. These results suggest that, in the innervated dog stomach, the enterogastrone action of fat is not primarily mediated by gastric inhibitory polypeptide.

Topics: Animals; Cholecystokinin; Dogs; Eating; Gastric Fistula; Gastric Inhibitory Polypeptide; Gastric Juice; Gastrins; Gastrointestinal Hormones; Oleic Acids; Pancreatic Fistula; Pancreatic Juice; Pentagastrin; Secretin

By means of a newly developed device, secretory response of the exocrine pancreas to feeding was continuously recorded for 24 h in conscious dogs. It was then found that the postprandial secretory pattern of the pancreas was biphasic. The first peak of secretion, rich in enzymes, occurred 2.3 +/- 0.11 h after feeding and its secretory volume was 25.3 +/- 3.10 ml/h. After the first peak, pancreatic secretion decreased slightly, but started to increase again. At 10.8 +/- 0.31 h after feeding, the second peak of secretion occurred and this was 40.5 +/- 2.93 ml/h, significantly higher than the first peak secretion and the greatest in 1 day. The second peak secretion did not contain a higher concentration of enzymes, but was rich in bicarbonate. Approximately 16 h after feeding, pancreatic secretion returned to the basal level, which continued until the next meal. That water and bicarbonate secretion of the pancreas is the greatest at about the 11th postprandial h had never been reported before. The physiological role of the pancreatic secretion at that time is more likely to be related to the neutralization of acid entering from the stomach than to the digestion of food.

Topics: Animals; Cholecystokinin; Circadian Rhythm; Dogs; Dose-Response Relationship, Drug; Feeding Behavior; Pancreas; Pancreatic Fistula; Pancreatic Juice; Secretin; Time Factors

In 4 dogs with pancreatic and gastric fistulae the effect of somatostatin (SST) on the pancreas was investigated during stimulation by pancreozymin-secretin or by a test meal. The pancreozymin-secretin-induced enzyme output and bile flow, as well as the enzyme concentration and duodenal volume during test meal stimulation were significantly reduced by SST. SST caused a less marked decrease in bicarbonate concentration, while volume and bicarbonate output did not change.

Topics: Animals; Bicarbonates; Cholecystokinin; Dogs; Gastric Fistula; Pancreas; Pancreatic Fistula; Secretin; Somatostatin

The nature and extent of growth hormone-release inhibiting hormone (GH-RIH, somatostatin)-induced inhibition of pancreatic secretion of bicarbonate and protein, an index of enzyme secretion, were studied by administration of exogenous secretin or cholecystokinin (CCK) and of a number of stimulants for endogenous release of these hormones in fasted pancreatic fistula dogs with and without an infusion of GH-RIH. The results of this study show that GH-RIH inhibits the pancreatic fluid and bicarbonate secretion induced by duodenal acidification and exogenous secretion. The kinetic analysis shows that the interaction between GH-RIH and secretin affecting pancreatic bicarbonate secretion possesses the characteristics of competitive inhibition. GH-RIH does not change the pancreatic protein response to exogenous CCK, but profoundly inhibits pancreatic response to a variety of the endogenous stimulants of CCK release, including duodenal perfusion of sodium oleate, amino acid mixture, or feeding of a peptone meal. We conclude that GH-RIH is a very potent inhibitor of the endogenous release of CCK from the intestinal mucosa and inhibits competitively the action of secretin but not CCK on the exocrine pancreatic secretion.

Topics: Animals; Bicarbonates; Cholecystokinin; Depression, Chemical; Dogs; Dose-Response Relationship, Drug; Gastric Fistula; Gastric Juice; Oleic Acids; Pancreas; Pancreatic Fistula; Peptides; Proteins; Secretin; Somatostatin

In dogs provided with chronic gastric and pancreatic fistulas (Thomas cannula), an 80-minute intraduodenal CaCl2 (0.6 mM/kg.) infusion against a background of secretin perfusion (GIH, 1.0 CU/kg./hr.) elicits a complex "pancreon" response consisting of both excitatory and inhibitory effects on the protein and alkaline components, respectively, of pancreatic secretion. It is postulated that these pancreatic secretion changes are the result of the interplay of released CCK and calcitonin. The lack of pancreatic secretion modifications when ethanol (0.7 mg./kg.) was added to the intraduodenal CaCl2 infusion suggests that the former counteracts the effects of the latter on the nerves and/or the endocrine cells of the gut. Ca++ concentration and output in pancreatic secretion did not change significantly either with the intraduodenal CaCl2 alone or associated with ethanol. Fasting blood Ca++ levels were not modified either by the secretin perfusion or by the intraduodenal CaCl2 infusion, either given alone or associated with ethanol.

Topics: Alkalies; Animals; Calcitonin; Calcium; Calcium Chloride; Cholecystokinin; Chronic Disease; Dogs; Duodenum; Ethanol; Gastric Fistula; Infusions, Parenteral; Pancreas; Pancreatic Fistula; Pancreatic Juice; Proteins; Secretin

Topics: Animals; Cholecystokinin; Diazoxide; Male; Pancreas; Pancreatic Fistula; Rats

Vasoactive inhibitory peptide (VIP) and secretin were compared in regard to the stimulation of pancreatic bicarbonate secretion and the augmentation of pancreatic response to caerulein or a peptone meal in chronic gastric and pancreatic fistula dogs. Dose-response analysis showed that maximal bicarbonate response to VIP was about 17% of that to secretin. Both caerulein and endogenous cholecystokinin, released by a peptone meal, clearly potentiated pancreatic bicarbonate response to VIP in a manner similar to secretin. The interactions of these two peptides showed that VIP is a potent inhibitor of secretin-induced pancreatic secretion. From the dose-response curves to secretin alone and secretin plus VIP, Michaelis-Menten analysis showed typical competitive inhibition, which indicates that VIP and secretin share a common receptor site.

Topics: Amylases; Animals; Bicarbonates; Ceruletide; Cholecystokinin; Depression, Chemical; Dogs; Dose-Response Relationship, Drug; Drug Combinations; Drug Synergism; Gastric Fistula; Gastrointestinal Hormones; Infusions, Parenteral; Kinetics; Pancreas; Pancreatic Fistula; Pancreatic Juice; Peptides; Peptones; Proteins; Secretin

Topics: Animals; Bicarbonates; Cholecystokinin; Depression, Chemical; Dogs; Ethanol; Gastric Fistula; Injections, Intravenous; Lipase; Pancreas; Pancreatic Fistula; Pancreatic Juice; Proteins; Secretin; Secretory Rate; Stimulation, Chemical; Stomach

Topics: Animals; Bicarbonates; Cholecystokinin; Dogs; Duodenum; Gastric Fistula; Hydrochloric Acid; Leucine; Pancreas; Pancreatic Fistula; Pancreatic Juice; Secretin; Stomach; Tryptophan

Topics: Amino Acids; Animals; Bicarbonates; Cholecystokinin; Denervation; Depression, Chemical; Dogs; Duodenum; Female; Gastric Fistula; Gastric Juice; Gastric Mucosa; Gastrointestinal Hormones; Hydrogen-Ion Concentration; Intestinal Secretions; Pancreas; Pancreatic Fistula; Pentagastrin; Phenylalanine; Proteins; Secretin; Stimulation, Chemical; Stomach

Topics: Animals; Cholecystokinin; Dogs; Dose-Response Relationship, Drug; Duodenum; Gastric Fistula; Glucagon; Injections, Intravenous; Leucine; Pancreas; Pancreatic Fistula; Pancreatic Juice; Proteins; Tryptophan

Topics: Animals; Biological Transport; Body Water; Cholecystokinin; Duodenum; Injections; Injections, Intraperitoneal; Intestinal Absorption; Male; Pancreas; Pancreatic Fistula; Pancreatic Juice; Rats; Spectrophotometry, Ultraviolet; Trypsin; Trypsin Inhibitors

Topics: Animals; Bethanechol Compounds; Ceruletide; Cholecystokinin; Dogs; Dose-Response Relationship, Drug; Gastric Fistula; Gastrointestinal Agents; Histamine; Pancreas; Pancreatic Fistula; Peptides; Proteins; Secretory Rate; Stimulation, Chemical; Stomach; Vagotomy

Topics: Animals; Bicarbonates; Blood Volume; Cholecystokinin; Chymotrypsin; Dogs; Dose-Response Relationship, Drug; Gastric Fistula; Infusions, Parenteral; Isoproterenol; Pancreas; Pancreatic Elastase; Pancreatic Fistula; Propranolol; Secretin; Trypsin

Topics: Alcoholism; Animals; Bicarbonates; Calculi; Cholecystokinin; Depression, Chemical; Dogs; Drug Synergism; Ethanol; Humans; Pancreas; Pancreatic Diseases; Pancreatic Fistula; Pancreatic Juice; Proteins; Secretin; Stimulation, Chemical

Topics: Analysis of Variance; Animals; Bicarbonates; Biliary Fistula; Cholecystokinin; Dose-Response Relationship, Drug; Drug Interactions; Male; Pancreas; Pancreatic Fistula; Pancreatic Juice; Rats; Secretin; Stimulation, Chemical

Topics: Animals; Atropine; Bicarbonates; Cholecystokinin; Depression, Chemical; Dogs; Ethanol; Gastric Fistula; Infusions, Parenteral; Isotonic Solutions; Lipase; Pancreas; Pancreatic Fistula; Pancreatic Juice; Proteins; Secretin; Secretory Rate; Sodium Chloride

Topics: Animals; Bethanechol Compounds; Ceruletide; Cholecystokinin; Dogs; Gastric Fistula; Gastric Juice; Gastric Mucosa; Gastrointestinal Agents; Leucine; Pancreas; Pancreatic Fistula; Pancreatic Juice; Pentagastrin; Peptides; Stomach; Tryptophan

Topics: Animals; Atropine; Bicarbonates; Cholecystokinin; Dogs; Duodenum; Gastric Fistula; Injections, Intravenous; Leucine; Pancreas; Pancreatic Fistula; Proteins; Secretin; Tryptophan

Topics: Animals; Bicarbonates; Cats; Cholecystokinin; Drug Synergism; Female; Gastric Fistula; Hydrochloric Acid; Pancreas; Pancreatic Fistula; Pancreatic Juice; Phenylalanine; Secretin

Topics: Acetylcholine; Animals; Carbon; Carbon Isotopes; Cholecystokinin; Histidine; Male; Pancreas; Pancreatic Fistula; Pancreatic Juice; Protein Biosynthesis; Proteins; Secretin; Swine; Zinc; Zinc Isotopes

Topics: Animals; Cholecystokinin; Dogs; Female; Gastric Fistula; Gastric Juice; Gastric Mucosa; Hexoses; Histamine; Insulin; Male; Pancreas; Pancreatic Fistula; Pancreatic Juice; Secretin; Stimulation, Chemical; Vagus Nerve

Topics: Animals; Bicarbonates; Cholecystokinin; Dogs; Drug Synergism; Duodenum; Injections, Intravenous; Pancreas; Pancreatic Fistula; Phenylalanine; Proteins; Secretin; Stimulation, Chemical

Topics: Bethanechol Compounds; Catheterization; Cholecystokinin; Contrast Media; Humans; Injections, Intravenous; Male; Manometry; Middle Aged; Morphine; Nitroglycerin; Pain; Pancreatic Diseases; Pancreatic Ducts; Pancreatic Fistula; Pancreatitis; Pressure; Radiography

Topics: Acetates; Amino Acids; Amylases; Animals; Atropine; Cholecystokinin; Duodenum; Fatty Acids; Gastroenterostomy; Hydrochloric Acid; Imides; Lipase; Pancreatic Fistula; Pancreatic Juice; Pentolinium Tartrate; Proteins; Secretin; Swine

Topics: Animals; Bicarbonates; Cats; Cholecystokinin; Consciousness; Gastric Fistula; Gastric Juice; Injections, Intravenous; Pancreas; Pancreatic Fistula; Pancreatic Juice; Secretin; Secretory Rate

Topics: Animals; Cholecystokinin; Dogs; Elasticity; Gastric Fistula; Gastric Juice; Gastrins; Histamine; Insulin; Pancreatic Fistula; Pancreatic Juice; Pepsin A; Secretin; Stomach; Vagus Nerve; Water

Topics: Amylases; Animals; Atropine; Cholecystokinin; Dogs; Drug Synergism; Injections, Intravenous; Lipase; Methacholine Compounds; Pancreas; Pancreatic Fistula; Pancreatic Juice; Secretin

Topics: Animals; Carbachol; Cholecystokinin; Coloring Agents; Elastin; Enzyme Induction; Enzyme Precursors; Female; Male; Methacholine Compounds; Pancreatic Elastase; Pancreatic Fistula; Pancreatic Juice; Pilocarpine; Rats; Secretin; Trypsin

Topics: Animals; Cholecystokinin; Digestion; Dogs; Gastric Fistula; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Histamine; Pancreatic Fistula; Pancreatic Juice; Pharmacology; Pylorus; Research; Secretin; Stomach

Topics: Animals; Cholecystokinin; Dogs; Gastric Fistula; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Injections, Intravenous; Injections, Subcutaneous; Intestinal Mucosa; Pancreas; Pancreatic Fistula; Secretin; Tissue Extracts

Topics: Amylases; Animals; Bicarbonates; Cholecystokinin; Digestion; Dogs; Gastrointestinal Hormones; Injections; Injections, Intravenous; Pancreas; Pancreatic Fistula; Pancreatic Juice; Physiology; Research; Secretin

Topics: Animals; Cats; Cholecystokinin; Digestion; Dogs; Gastrointestinal Hormones; Pancreatic Extracts; Pancreatic Fistula; Pancreatic Juice; Physiology; Research; Secretin; Vagotomy

Topics: Cholecystokinin; Gastrointestinal Hormones; Humans; Pancreas; Pancreatic Cyst; Pancreatic Fistula; Pancreatic Neoplasms; Pancreatitis