Lipopolysaccharide-induced gastroprotection is independent of the vagus nerve

Yong S. Kim, Lily K. Chang, David W. Mercer

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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 ip) 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 ip) 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.

Original languageEnglish (US)
Article number342660
Pages (from-to)1526-1532
Number of pages7
JournalDigestive Diseases and Sciences
Volume46
Issue number7
DOIs
StatePublished - Jan 1 2001

Fingerprint

Vagus Nerve
Lipopolysaccharides
Stomach
Gastrins
Endotoxemia
Vagotomy
Atropine
Cholinergic Agents
Ethanol
Truncal Vagotomy
Wounds and Injuries
Radioimmunoassay
Lasers

Keywords

  • Blood flow
  • Cholinergic nerves
  • Gastric injury
  • Gastrin
  • Lipopolysaccharide
  • Vagus nerve

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

Cite this

Lipopolysaccharide-induced gastroprotection is independent of the vagus nerve. / Kim, Yong S.; Chang, Lily K.; Mercer, David W.

In: Digestive Diseases and Sciences, Vol. 46, No. 7, 342660, 01.01.2001, p. 1526-1532.

Research output: Contribution to journalArticle

@article{0e1b22f28fa64038a336c15827012b26,
title = "Lipopolysaccharide-induced gastroprotection is independent of the vagus nerve",
abstract = "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 ip) 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 ip) 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.",
keywords = "Blood flow, Cholinergic nerves, Gastric injury, Gastrin, Lipopolysaccharide, Vagus nerve",
author = "Kim, {Yong S.} and Chang, {Lily K.} and Mercer, {David W.}",
year = "2001",
month = "1",
day = "1",
doi = "10.1023/A:1010656324614",
language = "English (US)",
volume = "46",
pages = "1526--1532",
journal = "Digestive Diseases and Sciences",
issn = "0163-2116",
publisher = "Springer New York",
number = "7",

}

TY - JOUR

T1 - Lipopolysaccharide-induced gastroprotection is independent of the vagus nerve

AU - Kim, Yong S.

AU - Chang, Lily K.

AU - Mercer, David W.

PY - 2001/1/1

Y1 - 2001/1/1

N2 - 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 ip) 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 ip) 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.

AB - 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 ip) 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 ip) 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.

KW - Blood flow

KW - Cholinergic nerves

KW - Gastric injury

KW - Gastrin

KW - Lipopolysaccharide

KW - Vagus nerve

UR - http://www.scopus.com/inward/record.url?scp=0034947376&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034947376&partnerID=8YFLogxK

U2 - 10.1023/A:1010656324614

DO - 10.1023/A:1010656324614

M3 - Article

C2 - 11478506

AN - SCOPUS:0034947376

VL - 46

SP - 1526

EP - 1532

JO - Digestive Diseases and Sciences

JF - Digestive Diseases and Sciences

SN - 0163-2116

IS - 7

M1 - 342660

ER -