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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 62 (1984), S. 523-530 
    ISSN: 1432-1440
    Keywords: Neurotensin ; Gastrointestinal hormones ; Gastric secretion ; Pancreatic secretion ; Motility ; Insulin ; Glucagon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neurotensin is a tridecapeptide originally isolated and characterized from bovine hypothalamus and later, in identical form, from bovine and human intestine. In the rat about 85% of immunoreactive neurotensin is found in the gut and about 10% in the brain. When an antibody specific for the amino terminal region of neurotensin was used the highest concentrations were found in the mucosa of the ileum, while an antibody specific for the biologically active region, the carboxyl terminus, also detected large amounts in the mucosa of the upper gastrointestinal tract. After a meal neurotensin — as measured by carboxyl terminal antibodies — rises after 5 min, a time in which the chymus has not yet reached the ileum, the main source of whole neurotensin. It is therefore possible that the carboxyl terminal molecules of neurotensin, found in the upper gastrointestinal tract, play an important physiological role. In plasma, neurotensin is rapidly degraded into smaller amino terminal and therefore biologically inactive molecules. Increases of carboxyl terminal neurotensin have been found in plasma in only a very few studies. The nature of this immunoreactive material has not yet been established. Therefore, the physiological role of neurotensin as a circulating hormone is unknown. Potential actions of neurotensin include thermoregulation, regulation of hormone release from brain (pituitary hormones) and gut (glucagon, insulin, somatostatin, pancreatic polypeptide), increase of vascular permeability, vasodilatation, inhibition of gastric acid secretion, stimulation of pancreatic secretion and changes of gut motility from the fasting to the fed type.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 29 (1984), S. 12-18 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In conscious dogs with gastric and duodenal Thomas fistulas, we studied the effect of ethanol on plasma concentrations of gastrin. Ethanol was given either as an infusion into a peripheral vein (1.95 M, 200 ml/hr) or into the duodenum (0.95 M, 400 ml/hr) or as an intragastric bolus injection. The effect of the intragastric bolus injection of 200 ml of different concentrations (0.3 M, 1.7 M, 6.85 M) of ethanol was compared with that of equimolar solutions of urea and sucrose (0.3 M, 1.56 M), and with that of sodium taurocholate (0.06 M) and distilled water. The gastrin responses to an oral mixed-meat meal (35 g/kg) were also investigated. Intragastric bolus injection of isoosmolar *0.3 M) ethanol, but not of equimolar solutions of urea and sucrose or H2O, significantly (P〈0.05) increased plasma gastrin levels above basal. Hyperosmolar solutions of ethanol, urea, and sucrose as well as hypoosmolar sodium taurocholate produced a pronounced increase of plasma gastrin concentrations above basal. The comparison of the mean 2-hr integrated plasma gastrin responses (IRG) showed that ethanol (6.85 M), urea (6.85 M), and sodium taurocholate (0.06 M) are at least as potent stimuli of release of gastrin as the test meal used. Intraduodenal and intravenous infusion of ethanol did not significantly alter mean plasma gastrin concentrations. We conclude that in the dog ethanol, but not urea and sucrose, given in a concentration (0.3 M) which is known not to disrupt the gastric mucosal barrier, increases plasma gastrin levels. This release of gastrin by isoosmolar ethanol is not due to gastric distension and may be a specific effect of ethanol on the gastrin cells. Furthermore, the release of gastrin by hyperosmolar solutions of ethanol, sucrose, and urea is probably a nonspecific effect and due to damage of gastric mucosa. The effect of a hypoosmolar solution of sodium taurocholate, a well-known gastric mucosal barrier breaker, on gastrin release supports this hypothesis.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 29 (1984), S. 321-326 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A comparison was made between use of isotonic 0.15 M sodium chloride and 5.8 g/100 ml glucose solutions for measurement of gastric acid secretion by intragastric titration in normal and ulcer subjects. Glucose distention did not cause significantly different acid secretion than saline distention in either group. The total amounts of glucose entering the duodenum over the 3.5-hr study period were 99 g in normal subjects and 122 g in ulcer subjects. In normal subjects, circulating gastrin-related acid secretion curves were not significantly different during endogenous peptone and exogenous G-17 stimulation using either the glucose or the saline meals. This finding provides evidence that glucose meals of this size do not alter sensitivity to gastrin. With glucose meals, inhibition of gastric emptying caused retention of a sufficient volume in the stomach to permit accurate continuous intragastric titration. Saline meals caused pronounced diarrhea which was not seen after glucose meals. Glucose distention intragastric titration allows reliable comparisons of endogenously and exogenously stimulated gastric acid secretion without serious side effects and is especially suitable for studying acid secretion in duodenal ulcer subjects.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2568
    Keywords: pancreatic polypeptide ; vagus nerves ; splanchnic nerves ; pancreatic secretion ; atropine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of the sympathetic and parasympathetic innervation in the release of pancreatic polypeptide (PP) basally and in response to a meal was studied after stepwise extrinsic denervation of the pancreas and the upper gastrointestinal tract in conscious dogs with gastric fistulae. One set of seven dogs was fed a meat meal (35 g/kg body weight) before and after truncal vagotomy and after truncal vagotomy plus celiac and superior mesenteric ganglionectomy, ie, extrinsic denervation of the pancreas and the upper gastrointestinal tract. In another set of six dogs, only ganglionectomy was performed. Experiments were repeated in the presence of atropine (50 μg/kg body weight, given as an intravenous bolus 60 min prior to the meal). Truncal vagotomy significantly (P〈0.05) reduced the postprandial 120-min integrated plasma PP response (IPPPR) by 84% as compared to the prevagotomy response. Before truncal vagotomy, atropine significantly reduced the IPPPR by 57%. After truncal vagotomy, atropine completely abolished the residual PP response. Additional celiac and superior mesenteric ganglionectomy did not alter the IPPPR already reduced by truncal vagotomy. With the vagus nerves intact, ganglionectomy alone had no effect on the IPPPR whether or not atropine was given. These findings indicate that (1) the splanchnic nerves do not play a significant role in postprandial PP release and (2) that the vagus nerves are important mediators of the response to a meal. The effect of atropine on postprandial PP release after truncal vagotomy may be due to interruption of short enteropancreatic reflexes, suppression of the intrinsic cholinergic activity of the pancreas, or inhibition of hormonally induced PP release.
    Type of Medium: Electronic Resource
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