Effects of endotoxin on gastric injury from luminal irritants in rats: Potential roles of nitric oxide

David W. Mercer, Antonio A. Castaneda, Jeremy W. Denning, Lily Chang, Diane H. Russell

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

The expression and function of inducible nitric oxide synthase (iNOS) in the stomach is unclear. This study assessed the effects of endotoxin on rat gastric iNOS expression and its role in gastric injury from luminal irritants. In conscious rats, a 5-h treatment with intraperitoneal lipopolysaccharide (LPS; 1-20 mg/kg) dose dependently increased gastric mucosal iNOS immunoreactivity and increased gastric luminal nitrate and nitrite accumulation (Griess reaction). LPS also increased gastric luminal fluid accumulation and reduced macroscopic gastric injury from orogastric acidified ethanol. Aminoguanidine (45 mg/kg) did not prevent LPS-induced gastroprotection or gastric fluid accumulation. N(G)-nitro-L-arginine methyl ester increased gastric luminal fluid and caused macroscopic gastric injury when given with LPS. Using an anesthetized preparation followed by removal of luminal fluid, LPS reduced gastric mucosal blood flow and exacerbated gastric injury from either acidified ethanol or acidified taurocholate, an effect that was negated by aminoguanidine. These data indicate that in conscious rats, the gastroprotective effect of endotoxin is dependent on constitutive NOS but not iNOS activity. However, the inducible isoform participates in the ability of endotoxin to exacerbate gastric injury from luminal irritants in the anesthetized rat.

Original languageEnglish (US)
Pages (from-to)G449-G459
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume275
Issue number3 38-3
StatePublished - Sep 1 1998

Fingerprint

Irritants
Endotoxins
Stomach
Nitric Oxide
Wounds and Injuries
Nitric Oxide Synthase Type II
Ethanol
Taurocholic Acid
NG-Nitroarginine Methyl Ester
Nitrites
Nitrates
Lipopolysaccharides
Protein Isoforms

Keywords

  • Blood flow
  • Nitric oxide synthase

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

Cite this

Effects of endotoxin on gastric injury from luminal irritants in rats : Potential roles of nitric oxide. / Mercer, David W.; Castaneda, Antonio A.; Denning, Jeremy W.; Chang, Lily; Russell, Diane H.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 275, No. 3 38-3, 01.09.1998, p. G449-G459.

Research output: Contribution to journalArticle

Mercer, David W. ; Castaneda, Antonio A. ; Denning, Jeremy W. ; Chang, Lily ; Russell, Diane H. / Effects of endotoxin on gastric injury from luminal irritants in rats : Potential roles of nitric oxide. In: American Journal of Physiology - Gastrointestinal and Liver Physiology. 1998 ; Vol. 275, No. 3 38-3. pp. G449-G459.
@article{6da24bec0f07419988755f0321dbfea9,
title = "Effects of endotoxin on gastric injury from luminal irritants in rats: Potential roles of nitric oxide",
abstract = "The expression and function of inducible nitric oxide synthase (iNOS) in the stomach is unclear. This study assessed the effects of endotoxin on rat gastric iNOS expression and its role in gastric injury from luminal irritants. In conscious rats, a 5-h treatment with intraperitoneal lipopolysaccharide (LPS; 1-20 mg/kg) dose dependently increased gastric mucosal iNOS immunoreactivity and increased gastric luminal nitrate and nitrite accumulation (Griess reaction). LPS also increased gastric luminal fluid accumulation and reduced macroscopic gastric injury from orogastric acidified ethanol. Aminoguanidine (45 mg/kg) did not prevent LPS-induced gastroprotection or gastric fluid accumulation. N(G)-nitro-L-arginine methyl ester increased gastric luminal fluid and caused macroscopic gastric injury when given with LPS. Using an anesthetized preparation followed by removal of luminal fluid, LPS reduced gastric mucosal blood flow and exacerbated gastric injury from either acidified ethanol or acidified taurocholate, an effect that was negated by aminoguanidine. These data indicate that in conscious rats, the gastroprotective effect of endotoxin is dependent on constitutive NOS but not iNOS activity. However, the inducible isoform participates in the ability of endotoxin to exacerbate gastric injury from luminal irritants in the anesthetized rat.",
keywords = "Blood flow, Nitric oxide synthase",
author = "Mercer, {David W.} and Castaneda, {Antonio A.} and Denning, {Jeremy W.} and Lily Chang and Russell, {Diane H.}",
year = "1998",
month = "9",
day = "1",
language = "English (US)",
volume = "275",
pages = "G449--G459",
journal = "American Journal of Physiology - Renal Physiology",
issn = "0363-6127",
publisher = "American Physiological Society",
number = "3 38-3",

}

TY - JOUR

T1 - Effects of endotoxin on gastric injury from luminal irritants in rats

T2 - Potential roles of nitric oxide

AU - Mercer, David W.

AU - Castaneda, Antonio A.

AU - Denning, Jeremy W.

AU - Chang, Lily

AU - Russell, Diane H.

PY - 1998/9/1

Y1 - 1998/9/1

N2 - The expression and function of inducible nitric oxide synthase (iNOS) in the stomach is unclear. This study assessed the effects of endotoxin on rat gastric iNOS expression and its role in gastric injury from luminal irritants. In conscious rats, a 5-h treatment with intraperitoneal lipopolysaccharide (LPS; 1-20 mg/kg) dose dependently increased gastric mucosal iNOS immunoreactivity and increased gastric luminal nitrate and nitrite accumulation (Griess reaction). LPS also increased gastric luminal fluid accumulation and reduced macroscopic gastric injury from orogastric acidified ethanol. Aminoguanidine (45 mg/kg) did not prevent LPS-induced gastroprotection or gastric fluid accumulation. N(G)-nitro-L-arginine methyl ester increased gastric luminal fluid and caused macroscopic gastric injury when given with LPS. Using an anesthetized preparation followed by removal of luminal fluid, LPS reduced gastric mucosal blood flow and exacerbated gastric injury from either acidified ethanol or acidified taurocholate, an effect that was negated by aminoguanidine. These data indicate that in conscious rats, the gastroprotective effect of endotoxin is dependent on constitutive NOS but not iNOS activity. However, the inducible isoform participates in the ability of endotoxin to exacerbate gastric injury from luminal irritants in the anesthetized rat.

AB - The expression and function of inducible nitric oxide synthase (iNOS) in the stomach is unclear. This study assessed the effects of endotoxin on rat gastric iNOS expression and its role in gastric injury from luminal irritants. In conscious rats, a 5-h treatment with intraperitoneal lipopolysaccharide (LPS; 1-20 mg/kg) dose dependently increased gastric mucosal iNOS immunoreactivity and increased gastric luminal nitrate and nitrite accumulation (Griess reaction). LPS also increased gastric luminal fluid accumulation and reduced macroscopic gastric injury from orogastric acidified ethanol. Aminoguanidine (45 mg/kg) did not prevent LPS-induced gastroprotection or gastric fluid accumulation. N(G)-nitro-L-arginine methyl ester increased gastric luminal fluid and caused macroscopic gastric injury when given with LPS. Using an anesthetized preparation followed by removal of luminal fluid, LPS reduced gastric mucosal blood flow and exacerbated gastric injury from either acidified ethanol or acidified taurocholate, an effect that was negated by aminoguanidine. These data indicate that in conscious rats, the gastroprotective effect of endotoxin is dependent on constitutive NOS but not iNOS activity. However, the inducible isoform participates in the ability of endotoxin to exacerbate gastric injury from luminal irritants in the anesthetized rat.

KW - Blood flow

KW - Nitric oxide synthase

UR - http://www.scopus.com/inward/record.url?scp=0031655999&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031655999&partnerID=8YFLogxK

M3 - Article

C2 - 9724255

AN - SCOPUS:0031655999

VL - 275

SP - G449-G459

JO - American Journal of Physiology - Renal Physiology

JF - American Journal of Physiology - Renal Physiology

SN - 0363-6127

IS - 3 38-3

ER -