Linked Life Data

10759257

Source:http://linkedlifedata.com/resource/pubmed/id/10759257

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2000-4-20
pubmed:abstractText
The pathogenesis of stress-induced gastroduodenal mucosal injury is complex and incompletely understood. The aim of this investigation was to examine the involvement of gastric and duodenal capsaicin-sensitive neurons in mucosal damage associated with water-restraint stress (WRS) in rats. Following WRS, gastroduodenal mucosal injury was quantitated by macroscopic and microscopic methods. Calcitonin gene-related peptide (CGRP) content was measured by radioimmunoassay. WRS-induced mucosal erosive injury in the stomach and duodenum (40.9 +/- 4.2 and 5.1 +/- 0.6 mm2, respectively) was reduced significantly (by 88% and 67%, respectively) by acute intragastric capsaicin administration prior to WRS. In contrast, sensory denervation by chronic capsaicin significantly increased the area of gastric injury and duodenal damage. WRS alone caused a significant reduction (by 52% and -35%, respectively) in gastric and duodenal CGRP content, which was prevented by acute capsaicin treatment. The data suggest that gastric and duodenal sensory neurons and CGRP are involved in the pathogenesis of stress-induced mucosal injury to the stomach and duodenum.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0163-2116
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
830-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Involvement of capsaicin-sensitive sensory neurons in stress-induced gastroduodenal mucosal injury in rats.
pubmed:affiliation
Department of Medicine, University of Oklahoma Health Sciences Center, and Oklahoma City Department of Veterans Affairs Medical Center, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.