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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2 Pt 1
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pubmed:dateCreated |
1996-12-20
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pubmed:abstractText |
This study was performed to identify the possible neural mechanisms and mediators that underlie the gastric mucosal hyperemia evoked by cholecystokinin octapeptide (CCK-8). Gastric mucosal blood flow in anesthetized rats was assessed by the clearance of hydrogen and gastric acid secretion determined in the luminally perfused stomach. The gastric mucosal hyperemic effect of a low dose of CCK-8 (0.04 nmol/min iv infusion for 7 min) was abolished by inhibition of nitric oxide synthesis with NG-nitro-L-arginine methyl ester (15 mg/kg iv) and significantly blunted by defunctionalization of afferent neurons with a neurotoxic dose of capsaicin (125 mg/kg sc). The hyperemic reaction to a high dose of CCK-8 (0.2 nmol/min) was not significantly affected by these pharmacological maneuvers. The vasodilator response to low-dose CCK-8 (0.04 nmol/min) was further analyzed and found to be inhibited by acute bilateral subdiaphragmatic vagotomy, atropine (1 mumol/kg ip), and the antagonistic calcitonin gene-related peptide (CGRP) fragment CGRP-(8-37) (6 nmol/ min ia). Cyclooxygenase inhibition with indomethacin (10 mg/kg ip) was ineffective. The CCK-8-induced increment of gastric acid secretion was not significantly altered by any of these procedures. These results indicate that the gastric vasodilator effect of submaximal doses of CCK-8 is brought about by a vagovagal reflex that involves acetylcholine, CGRP or a related peptide, and nitric oxide as vasodilator messengers.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcitonin Gene-Related Peptide,
http://linkedlifedata.com/resource/pubmed/chemical/Capsaicin,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Sincalide,
http://linkedlifedata.com/resource/pubmed/chemical/calcitonin gene-related peptide...
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
270
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
G253-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8779966-Animals,
pubmed-meshheading:8779966-Calcitonin Gene-Related Peptide,
pubmed-meshheading:8779966-Capsaicin,
pubmed-meshheading:8779966-Female,
pubmed-meshheading:8779966-Gastric Acid,
pubmed-meshheading:8779966-Gastric Mucosa,
pubmed-meshheading:8779966-Hyperemia,
pubmed-meshheading:8779966-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:8779966-Nervous System Physiological Phenomena,
pubmed-meshheading:8779966-Nitric Oxide,
pubmed-meshheading:8779966-Peptide Fragments,
pubmed-meshheading:8779966-Rats,
pubmed-meshheading:8779966-Rats, Sprague-Dawley,
pubmed-meshheading:8779966-Regional Blood Flow,
pubmed-meshheading:8779966-Sincalide,
pubmed-meshheading:8779966-Vagotomy
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pubmed:year |
1996
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pubmed:articleTitle |
CCK-evoked hyperemia in rat gastric mucosa involves neural mechanisms and nitric oxide.
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pubmed:affiliation |
Department of Experimental and Clinical Pharmacology, University of Graz, Austria.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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