Helicobacter pylori lipopolysaccharide-provoked injury to rat gastroduodenal microvasculature involves inducible nitric oxide synthase.

Abstract:

:The actions of a purified Helicobacter pylori lipopolysaccharide (3 mg x kg(-1), i.v.) on rat gastric antral and duodenal microvascular integrity (determined as radiolabelled albumin leakage) and the expression of the inducible nitric oxide (NO) synthase (iNOS; assessed by the citrulline assay) were investigated 4 h after challenge. Significant increases of albumin leakage and expression of iNOS in both antral and duodenal tissues were observed following challenge. Concurrent administration of the selective iNOS inhibitor, 1400W (N-(8-(aminomethyl)benzyl)-acetamidine; 0.2-1 mg x kg(-1), s.c.), with lipopolysaccharide, caused a dose-dependent attenuation of the gastric and duodenal albumin leakage. Thus, H. pylori lipopolysaccharide can initiate the expression of iNOS in the stomach and duodenum following systemic challenge, which can provoke gastroduodenal microvascular dysfunction.

journal_name

Eur J Pharmacol

authors

Kiss J,Lamarque D,Moran AP,Pozsár J,Morschl E,László F,Whittle BJ

doi

10.1016/s0014-2999(01)01008-1

keywords:

subject

Has Abstract

pub_date

2001-05-25 00:00:00

pages

175-9

issue

2-3

eissn

0014-2999

issn

1879-0712

pii

S0014299901010081

journal_volume

420

pub_type

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