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1.
Surgery ; 97(4): 415-9, 1985 Apr.
Article in English | MEDLINE | ID: mdl-3983816

ABSTRACT

The purpose of this study was to investigate the effect of pentobarbital, halothane, and chloralose anesthesia on the endogenous release of cholecystokinin-33 (CCK-33) in dogs prepared with duodenal fistulas. Release of CCK-33 was induced by intraduodenal infusion of a medium-chain triglyceride (corn oil, 1 gm/kg/hr). Plasma CCK-33 concentrations were measured by means of a specific radioimmunoassay. Pentobarbital and chloralose were administered intravenously, and halothane was administered by a vaporizer (semiclosed technique), with O2 and N2O used as carriers. No incidence of hypotension was found with the use of these anesthetic agents. Basal concentrations of plasma CCK-33 were elevated, although not significantly, during pentobarbital or chloralose anesthesia. In conscious dogs (control study), peak plasma CCK-33 concentrations of 529 +/- 53 pg/ml were measured 30 minutes after intraduodenal infusion of fat. Under pentobarbital anesthesia, peak plasma CCK-33 concentrations of 452 +/- 264 pg/ml were found 80 minutes after infusion of fat. Under halothane anesthesia, fat-induced release of CCK-33 was abolished, whereas chloralose anesthesia did not influence fat-induced release of CCK-33. These findings may have implications for the design of future studies of gastrointestinal physiology. In CCK-33 studies that require anesthesia, chloralose appears to be an appropriate anesthetic agent.


Subject(s)
Anesthetics/pharmacology , Cholecystokinin/metabolism , Anesthesia, General , Animals , Chloralose/pharmacology , Cholecystokinin/blood , Corn Oil , Dogs , Female , Halothane/pharmacology , Male , Oils , Pentobarbital/pharmacology , Radioimmunoassay
2.
Surg Gynecol Obstet ; 159(6): 557-61, 1984 Dec.
Article in English | MEDLINE | ID: mdl-6095475

ABSTRACT

The present study was done to compare endogenous cholecystokinin-33 release in response to physiologic stimuli (meal, fat) in pigs, dogs and man. Plasma levels of cholecystokinin-33 were monitored using a radioimmunoassay for cholecystokinin which detects only cholecystokinin-33 and cholecystokinin-39. Ingestion of a meal caused release of cholecystokinin-33 within five, 20 and 120 minutes in man, pigs and dogs, respectively. Intraduodenal administration of corn oil resulted in a significant release of cholecystokinin-33 within 20 minutes in dogs, pigs and man.


Subject(s)
Cholecystokinin/metabolism , Dietary Fats/pharmacology , Food , Adult , Animals , Corn Oil , Dietary Fats/administration & dosage , Dogs , Female , Humans , Intubation, Gastrointestinal , Male , Oils/administration & dosage , Oils/pharmacology , Peptide Fragments/blood , Radioimmunoassay , Sincalide/blood , Swine , Time Factors
3.
Digestion ; 27(2): 57-62, 1983.
Article in English | MEDLINE | ID: mdl-6195035

ABSTRACT

Dietary fiber inhibits pancreatic enzyme activity--i.e., trypsin, lipase and amylase--in buffer solutions and in human duodenal juice in vitro. It is well established that oral administration of trypsin inhibitor stimulates the secretion and growth of the rat pancreas. In the present study, trypsin inhibitor (Trasylol) as well as dietary fiber such as pectin of low (37%) methoxylic esterification and wheat bran were found to stimulate pancreatic enzyme secretion in acute experiments in conscious rats with bile-pancreatic fistulae. Feeding for 10 days with wheat bran resulted in increased pancreatic weight and in increased protein and trypsinogen content. Administration of pectin of high (73%) methylic esterification caused increased pancreatic protein content and that of low methylic esterification increased pancreatic trypsinogen activity/milligram tissue. The results suggest that pectin and wheat bran may interfere with the feedback regulation of pancreatic enzyme secretion exerted by intraluminal trypsin, and, like trypsin inhibitor, have a secretagogue and trophic effect on the pancreas.


Subject(s)
Dietary Fiber/pharmacology , Pancreas/physiology , Amylases/metabolism , Animals , Male , Organ Size/drug effects , Pancreas/drug effects , Pancreas/enzymology , Pancreas/surgery , Pancreatic Fistula/physiopathology , Pectins , Proteins/metabolism , Rats , Rats, Inbred Strains , Trypsin Inhibitors
4.
Ann Surg ; 194(3): 321-7, 1981 Sep.
Article in English | MEDLINE | ID: mdl-7271349

ABSTRACT

Although it is generally assumed that release of cholecystokinin (CCK) is the chief mechanism by which a fatty meal causes contraction of the gallbladder, measured release of CCK and gallbladder contraction have never been correlated. We have achieved this correlation in eight adult male volunteers, by means of a specific radioimmunoassay for CCK and by ultrasonographic imaging of the gallbladder. This study validates our CCK radioimmunoassay and correlates measured concentrations of CCK with changes in gallbladder size measured by ultrasonographic examination. Basal concentrations of CCK (82.6 +/- 10.4 pg/ml) rose significantly to a maximum of 411.1 +/- 79.9 pg/ml at 16 minutes after intraduodenal instillation of medium-chain triglyceride (Lipomul). Mean basal volume of the gallbladder was 34.6 cm3; maximum reduction of gallbladder volume (to one-third of original) was achieved at 18 minutes. Elevated CCK concentrations began to fall toward basal, and the gallbladder began to refill at 25 minutes. Results obtained after oral ingestion of Lipomul provide similar results. Linear regression analysis demonstrated excellent correlation between concentrations of CCK and gallbladder size during both contraction and relaxation phases. Future study of this correlation may be useful in patients with manifest dysfunction of the gallbladder, as well as in individuals known to be at risk of gallbladder disease.


Subject(s)
Cholecystokinin/metabolism , Gallbladder/physiology , Adult , Cholecystokinin/blood , Corn Oil , Humans , Intestinal Mucosa/metabolism , Male , Middle Aged , Muscle Contraction , Oils , Radioimmunoassay , Ultrasonography , Zea mays
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