Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2001-7-31
pubmed:abstractText
This study was done to examine the role of the vagus nerve in a model of gastric injury during endotoxemia. In conscious rats, lipopolysaccharide (LPS; 20 mg/kg i.p.) treatment for 5 hr prevented macroscopic gastric injury caused by acidified ethanol (150 mM HCl/50% ethanol). In addition, LPS enhanced gastric luminal fluid accumulation, decreased gastric mucosal blood flow (laser Doppler), and increased plasma gastrin levels (radioimmunoassay). Subdiaphragmatic truncal vagotomy, performed 7 days prior to LPS inhibited LPS-induced fluid accumulation, further reduced gastric mucosal blood flow following LPS, and augmented LPS-induced gastrin release compared to those in pyloroplasty controls. Atropine (1 mg/kg i.p.) prevented LPS-induced fluid accumulation but did not influence the effects of LPS on blood flow or gastrin release. Neither vagotomy nor atropine negated LPS-induced gastroprotection. This is the first report to examine the role of cholinergic nerves in the stomach during endotoxemia. The data indicate that LPS causes accumulation of gastric luminal fluid in part through its effects on cholinergic nerves. In contrast, the effects of vagotomy on blood flow and gastrin release following LPS involve a noncholinergic pathway. However, LPS-induced gastroprotection is independent of the vagus nerve.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0163-2116
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1526-32
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Lipopolysaccharide-induced gastroprotection is independent of the vagus nerve.
pubmed:affiliation
Department of Surgery, University of Texas-Houston Medical School, 77026, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.