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  • dog  (2)
  • α-difluoromethylornithine  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Terbutaline, A β2-Adrenoreceptor agonist, inhibits gastric acid secretion and stimulates release of peptide YY and gastric inhibitory polypeptide in dogs (1990)
    Springer
    Digestive diseases and sciences 35 (1990), S. 453-457 
    Details
    ISSN: 1573-2568
    Keywords: terbutaline ; acid secretion ; peptide YY ; gastric inhibitory polypeptide ; dog
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Terbutaline, a β2-adrenoreceptor agonist, inhibits pentagastrin-stimulated gastric acid secretion. The purpose of this study was to examine the effect of intravenous administration of terbutaline on plasma levels of peptide YY(PYY) and gastric inhibitory polypeptide (GIP), both of which are known to inhibit gastric acid secretion. Seven dogs with gastric and duodenal fistulas were given pentagastrin (1 μg/kg/hr) intravenously for 150 min in combination with terbutaline (10 or 20 μg/kg/hr) or saline during the 60- to 120-min period of pentagastrin infusion. Pentagastrin-stimulated gastric acid secretion was significantly (P 〈0.05) inhibited by intravenous administration of terbutaline. Terbutaline significantly increased plasma PYY levels, 24% in response to terbutaline at 10 μg/kg/hr, and 59% at 20 μg/kg/hr. Plasma GIP levels were also increased significantly, 24% with terbutaline at 10 μg/kg/hr, and 39% at 20 μg/kg/hr. Our data suggest that terbutaline-induced inhibition of pentagastrin-stimulated gastric acid secretion is mediated, at least in part, by the release of PYY and GIP. The adrenergic nervous system may influence gastric acid secretion through the release of PYY and GIP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01536919
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Species-specific effects of neurotensin on gallbladder contractionin vitro (1989)
    Springer
    Digestive diseases and sciences 34 (1989), S. 21-26 
    Details
    ISSN: 1573-2568
    Keywords: neurotensin ; gallbladder contraction ; sphincter of Oddi ; dog
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have previously shown that an in vivoadministration of neurotensin (NT) stimulates contraction of dog gallbladder (GB), but produces dilatation of GB in humans. The objective of this study was to examine the effect of NT on human, dog, guinea pig, and rabbit GB in vitro,in order to delineate direct versus indirect actions of NT in different species and to evaluate the structure-activity relationships of NT. The effect of NT on the canine sphincter of Oddi (SOD) was also examined in vitro.Isolated longitudinal strips of GB from the four species given above and SOD from dogs were suspended in oxygenated Krebs buffer, and the isometric tension responses to various doses of NT, NT 8–13, NT 1–11, and xenopsin (XP) were determined. All the NT homologs, except NT 1–11, stimulated contraction of the dog GB and SOD in a dose-dependent manner. NT also caused dose-related stimulation of GB contraction from guinea pigs but did not stimulate or depress the contractile activity of human and rabbit GB strips. These results suggest that NT action on GB contraction is species-specific. Tetrodotoxin did not modify the contraction of dog GB and SOD in response to NT, indicating that NT mediates its contractile effects directly. The relaxing effect of NT on GB of humans in vivo,as previously reported by us, thus appears to be an indirect action. The fact that structural changes in the NT molecule resulted in marked changes in the biological activity of NT on GB activity in dogs indicates that the effects of NT on dog GB contraction are probably mediated through binding of NT to specific receptors that requires both the C-terminal amino group and the two C-terminal amino acids to produce a contractile response. Based on these results, we suggest that NT may participate in the regulation of GB and SOD contraction in dogs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01536149
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Cyclosporine and α-difluoromethylornithine exhibit differential effects on colon and pancreatic cancer in vitro (1987)
    Springer
    Investigational new drugs 5 (1987), S. 251-258 
    Details
    ISSN: 1573-0646
    Keywords: cancer ; cyclosporine ; pancreas ; colon ; polyamines ; α-difluoromethylornithine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract α-Difluoromethylornithine (DFMO) is a known irreversible inhibitor of ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis. Cyclosporine (CsA) has been reported to inhibit ODC activity in vitro. In the present study, we compared the effects of DFMO and CsA on growth, survival, and polyamine levels in mouse colon cancer (MC-26) and hamster pancreatic cancer (H2T) cells in vitro. The growth and survival of MC-26 and H2T cells were inhibited by both DFMO and CsA. However, H2T cells were observed to be significantly more sensitive than MC-26 cells to both CsA and DFMO. The inhibitory effects of CsA were blocked by the addition of the polyamine, putrescine, in both MC-26 and H2T cells. Polyamine levels were altered significantly in both MC-26 and H2T cells treated with CsA and DFMO. However, the profile of these alterations differed between MC-26 and H2T cell lines. Putrescine and spermidine levels in MC-26 cells were more sensitive to DFMO inhibition than were H2T cells. Spermine levels were consistently elevated in MC-26 cells exposed to CsA or DFMO, while the level of spermine in H2T cells decreased significantly in response to the same drugs. These results suggest that CsA and DFMO exhibit different effects on colon and pancreatic cancer growth in vitro. In addition, the differences in the sensitivity of pancreatic and colon cancer to CsA and DFMO indicate potentially important differences in polyamine metabolism between the two cell lines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175295
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  • 4
    Electronic Resource
    Electronic Resource
    2-deoxy-D-glucose inhibits the antitumor effects of α-difluoromethylornithine on the growth of colon cancer in vivo (1989)
    Springer
    Investigational new drugs 7 (1989), S. 131-138 
    Details
    ISSN: 1573-0646
    Keywords: polyamines ; cancer ; 2-deoxy-D-glucose ; α-difluoromethylornithine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The glycolytic inhibitor, 2-deoxy-D-glucose (2-DG), has been shown to inhibit the growth of certain cancers. α-Difluoromethylornithine (DFMO) is an irreversible inhibitor of ornithine decarboxylase (ODC), the ratelimiting enzyme in polyamine biosynthesis. DFMO has been shown to inhibit cancer growth in a number of models. The present study was designed to investigate the effects of 2-DG alone and combined with DFMO on MC-26 mouse colon adenocarcinoma tumors growing in vivo. Twenty-eight male Balb/c mice were inoculated with 250,000 MC-26 cells, and then randomized into four groups of 7 each: group I served as control; group II received DFMO (3% in drinking water); group III received 2-DG (500 mg/kg/d IP); group IV received a combination of 2-DG and DFMO. Treatment began 5 days after tumor cell inoculation. MC-26 tumor area was reduced 73% by DFMO compared to a 24% reduction caused by 2-DG. The tumor weight was reduced 80% by DFMO and 52% by 2-DG. The tumor contents of DNA, RNA, and protein were significantly reduced by DFMO but not 2-DG. The tumor concentration of the polyamines putrescine and spermidine were reduced by DFMO alone or combined with 2-DG while spermine levels remained unchanged. 2-DG alone did not alter polyamine levels. These results indicate that both 2-DG and DFMO, when added as single agents, inhibit tumor growth. However, the addition of 2-DG to the DFMO regimen inhibited the antitumor effects of DFMO. Survival studies performed on MC-26 cells in vitro corroborated the antagonisms between DFMO and 2-DG that were shown in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170849
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    Paper (German National Licenses)
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