Influence of Helicobacter pylori infection on in vitro responsiveness of gastric fundus to agonists and to stimulation of enteric nerves in Mongolian gerbils.
BACKGROUND
It has recently been proposed that disturbed gastric adaptive relaxation may play a role in functional dyspepsia (FD). However, the effect of Helicobacter pylori infection, which may be one of multiple factors associated with FD, on gastric relaxation is not clear. The aim of this study was to clarify the influence of H. pylori infection on the responsiveness of smooth muscles of the gastric fundus to agonists or to stimulation of enteric nerves, with particular emphasis on nonadrenergic noncholinergic (NANC) relaxation.


METHODS
We investigated myogenic responses to carbachol (CCH) and sodium nitroprusside (SNP), and neural responses to electrical field stimulation (EFS), in the absence or presence of atropine and guanethidine, in the tissues of the gastric fundus of H. pylori-infected Mongolian gerbils (MGs).


RESULTS
H. pylori-infected MGs showed typical gastritis, with H. pylori colonization in the antrum and body. The gastric fundus adjacent to the body was composed of thin gastric mucosa with mild inflammation, which was covered with stratified squamous epithelium, and the muscle layer communicated with that of the gastric body. In the gastric fundus, CCH- and SNP-induced responses were not different in controls and H. pylori-infected MGs. In the absence of any antagonists, EFS-evoked contraction tended to be reduced in H. pylori-infected MGs compared with that in control MGs, albeit that the difference was statistically nonsignificant. N(omega)-nitro- l-arginine methyl ester inhibited NANC relaxation in the tissues in both groups. EFS-evoked NANC relaxation remained intact in H. pylori-infected MGs.


CONCLUSIONS
Mild inflammation in gastric fundus associated with H. pylori infection does not cause enteric neuromuscular dysfunction of the site in vitro.
Second Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan.
Yusuke
Y
Takehara
Yohei
Y
Mizuta
Hajime
H
Isomoto
Ken
K
Ohnita
Masaya
M
Yoshimura
Takashi
T
Nakamura
Fuminao
F
Takeshima
Katsuhisa
K
Omagari
Kunihiko
K
Murase
Ikuo
I
Murata
Kohtaro
K
Taniyama
Shigeru
S
Kohno
D000818:Animals; D002217:Carbachol / Q000494:pharmacology*; D018679:Cholinergic Agonists / Q000494:pharmacology*; D004415:Dyspepsia / Q000503:physiopathology*; D005748:Gastric Fundus / Q000187:drug effects* / Q000502:physiology; D005756:Gastritis / Q000473:pathology; D005769:Gastrointestinal Motility / Q000187:drug effects*; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000503:physiopathology*; D016480:Helicobacter pylori; D008297:Male; D020030:Nitric Oxide Donors / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology*
D018679:Cholinergic Agonists; D020030:Nitric Oxide Donors; D009599:Nitroprusside; D002217:Carbachol