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  • 1
    Electronic Resource
    Electronic Resource
    Stimulation of gastric secretion and enhanced gastric mucosal damage following central administration of pancreatic polypeptide (PP) in rats (1994)
    Springer
    Digestive diseases and sciences 39 (1994), S. 2398-2406 
    Details
    ISSN: 1573-2568
    Keywords: central nervous system ; gastric secretion ; gastric ulcer ; indomethacin ; intracisternal injection ; pancreatic polypeptide ; vagotomy ; 2-deoxy-d-glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was carried out to investigate the central effects of pancreatic polypeptide on gastric secretion and gastric ulcer formation in conscious rats. Intracisternal injection of rat pancreatic polypeptide (62.5, 250, and 1000 ng/rat) into pylorus-ligated rats resulted in a dose-dependent stimulation of gastric acid and pepsin secretion. In contrast, intraperitoneal injection of even higher doses of pancreatic polypeptide (250, 1000, and 2500 ng/rat) failed to increase gastric secretion. This stimulatory effect of centrally administered pancreatic polypeptide was completely blocked by vagotomy and by pretreatment with atropine. Intracisternal injection of PP (500–2000 ng/rat) dose-dependently increased the severity of gastric lesions induced by 2-deoxy-d-glucose or indomethacin. In contrast, intraperitoneal injection of PP failed to increase the severity of the gastric lesions induced by 2-deoxy-d-glucose or indomethacin. These results indicate that pancreatic polypeptide is capable of acting centrally in the brain to stimulate gastric acid and pepsin secretion through a vagal, muscarinic pathway and in so doing exerts an ulcerogenic action on the gastric mucosa.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02087657
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Gastric Emptying in OLETF Rats Not Expressing CCK-A Receptor Gene (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 915-919 
    Details
    ISSN: 1573-2568
    Keywords: GASTRIC EMPTYING ; CCK-A RECEPTOR ; OLETF RAT
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have very recently demonstrated the lowacidity of gastric juice and the high susceptibility tothe development of gastric ulceration in OtsukaLong-Evans Tokushima Fatty (OLETF) rats not expressing CCK-A receptors. In the present study, gastricemptying in this strain was examined and compared withcontrol Long-Evans Tokushima Otsuka (LETO) rats. Gastricemptying was evaluated by the phenol red method. Gastric emptying 30 and 60 min after a liquidmeal in OLETF rats was significantly delayed compared tothat in control LETO rats. Intraperitoneal injection ofCCK-8 at a dose of 5 μg/kg significantly inhibited gastric emptying in control LETO rats, whereasthe same dose of CCK-8 failed to inhibit gastricemptying in OLETF rats. These results suggest for thefirst time that gastric emptying was suppressed in OLETF rats. We also confirmed with this mutant thatCCK delays gastric emptying through the CCK-Areceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018860313674
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Case Report: Increased Serum Leptin by Cholecystitis in a Diabetic Patient (2000)
    Springer
    Digestive diseases and sciences 45 (2000), S. 933-936 
    Details
    ISSN: 1573-2568
    Keywords: cholecystitis ; leptin ; bacterial infection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005525108518
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Delayed Gastric Emptying by Helicobacter pylori Lipopolysaccharide in Conscious Rats (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 90-94 
    Details
    ISSN: 1573-2568
    Keywords: HELICOBACTER PYLORI ; LIPOPOLYSACCHARIDE ; GASTRIC EMPTYING
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was carried out to investigatethe possibility that lipopolysaccharide deprived fromHelicobacter pylori may alter gastric motility. Toaddress the question, we examined the effect of H. pylori lipopolysaccharide on gastricemptying in conscious rats. Gastric emptying wasevaluated by the phenol red method. Time-course anddose-related effects of intraperitoneal administrationof H. pylori lipopolysaccharide were investigated.Intraperitoneal injection of H. pylorilipopolysaccharide significantly suppressed gastricemptying of a liquid meal in a dose-dependent manner.The inhibitory action of H. pylori lipopolysaccharide wasobserved 2, 4, 8, or 12 hr after the injection. Theseresults suggest for the first time that H. pylorilipopolysaccharide may suppress gastric emptying in along-lasting fashion. It is also suggested that H. pylorimay influence gastric function through its cell wallstructure named lipopolysaccharide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018828105226
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Intraduodenal lipid does not inhibit acid secretion in OLETF rats not expressing CCK-A receptor gene (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 2174-2179 
    Details
    ISSN: 1573-2568
    Keywords: gastric acid secretion ; CCK-A receptor ; OLETF rat ; lipid ; pylorus ligation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Gastric acid secretion in response to pylorus-ligation and duodenal fat feeding in Otsuka Long-Evans Tokushima Fatty (OLETF) rats without cholecystokinin-A receptor was examined. Acidity of gastric juice obtained from pylorus-ligated OLETF rats was significantly lower than that of control LETO rats. Gastric acid secretion in response to bethanechol, pentagastrin, or atropine was maintained in both OLETF and LETO rats. Intraduodenal lipid injection strongly inhibited gastric acid secretion in control LETO rats. In contrast, administration of lipid into the duodenum failed to inhibit acid secretion in OLETF rats. These results suggest that basal gastric acid secretion may be impaired in OLETF rats and that the cholecystokinin-A receptor is involved in lipid-induced acid inhibition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02071397
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  • 6
    Electronic Resource
    Electronic Resource
    Evidence that gastric antisecretory action of lipopolysaccharide is not due to a toxic effect on gastric parietal cells (1992)
    Springer
    Digestive diseases and sciences 37 (1992), S. 1039-1044 
    Details
    ISSN: 1573-2568
    Keywords: endotoxin ; gastric acid secretion ; gastric parietal cell ; interleukin-1 ; lipopolysaccharide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have recently found that bacterial lipopolysaccharide (LPS) or endotoxin at minute doses inhibits the secretion of gastric acid and pepsin in rats. The present study was performed to determine whether this antisecretory action of LPS was a reversible biological response or a result of the destruction of gastric parietal cells by endotoxin. The intraperitoneal injection of LPS into pylorus-ligated rats resulted in a dose-related (40–4000 ng/kg) decrease in gastric acid secretion, with maximal inhibition being observed at a dose of 4000 ng/kg. The stomach then was examined both macroscopically and microscopically for the presence or absence of mucosal lesions or damaged gastric parietal cells. No morphological changes in the gastric mucosal, structure including parietal cells were observed even in the rats injected with 4000 ng/kg of LPS. Next, basal gastric acid output was compared in the rats that had received LPS (4000 ng/kg, intraperitoneal) or saline alone 24 hr before. There was no significant difference in gastric, acid secretion between the saline- and LPS-pretreated groups, indicating that the secretory capacity of gastric parietal cells returned to the control level at 24 hr after the injection of a maximal antisecretory dose of LPS. These results clearly suggest that the LPS-induced inhibition of gastric secretion results not from its toxic or destructive effect on the gastric secretory mechanism but from its reversible biological effect on gastric physiology.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01300284
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    Paper (German National Licenses)
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