Endoscopy 2000; 32(4): 294-299
DOI: 10.1055/s-2000-7383
Original Article
Georg Thieme Verlag Stuttgart ·New York

Gastric Mucosal Damage Caused by Monochloramine in the Rat and Protective Effect of Taurine: Endoscopic Observation Through Gastric Fistula

M. Kodama, H. Tsukada, M. Ooya, M. Onomura, T. Saito, K. Fukuda, H. Nakamura, T. Taniguchi, M. Tominaga, M. Hosokawa, J. Fujita, Y. Seino
  • Department of Metabolism and Clinical Nutrition, Faculty of Medicine, Kyoto University, Kyoto, Japan
Further Information

Publication History

Publication Date:
31 December 2000 (online)

Preview

Background and Study Aims: The mechanism of Helicobacter pylori-induced gastric mucosal injury is unknown, but H. pylori infection is conducive to accumulation in the stomach of monochloramine, a cytotoxic substance. The present study involved morphological investigation of the damaging effects of monochloramine on rat gastric mucosa, using endoscopic observations through a gastric fistula. The study also examined the protective effect of taurine against monochloramine-induced gastric mucosal lesions in rats.

Materials and Methods: The effects of monochloramine in rats were studied by administering the substance via a gastrostomy, which was then used to conduct a series of endoscopic observations. Local blood flow was measured using a laser Doppler method. Histological examination was carried out after 24 hours. Various monochloramine concentrations were used, and some animals were pretreated with taurine, a monochloramine scavenger, via the gastrostomy.

Results: Endoscopically, monochloramine was found to produce hemorrhagic mucosal erosions, mainly in the gastric body, in a time-dependent and concentration-dependent manner. Blood flow was decreased in advance of mucosal erosion. Taurine prevented mucosal injury by 30 mM monochloramine, the highest concentration tested.

Conclusions: Although only the first 24 hours of mucosal injury were observed in the present study, the most likely mechanisms by which monochloramine caused injury to the gastric mucosa appeared to be both oxidative damage and a reduction in blood flow, impairing the mucosal defense mechanism.

References

M.D. M. Kodama

Dept. of Metabolism and Clinical Nutrition Faculty of Medicine Kyoto University

54, Kawahara-cho, Sakyo-ku

Kyoto City 606-8507

Japan

Phone: + 81-75-751-4244