• Masahiko Inamori, Takeshi Shimamura, Hajime Nagase, Yasunobu Abe, Tadashi Umezawa, Atsushi Nakajima, Toshifumi Saito, Norio Ueno, Katsuaki Tanaka, Hisahiko Sekihara, Jun-ichi Togawa, Hiroki Kaifu, Hideo Tsuboi, Hideyuki Kayama, and Shizuo Tominaga.
• Third Department of Internal Medicine, Yokohama City University, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan. inamorim@med.yokohama-cu.ac.jp
• Hepato Gastroenterol. 2006 May 1; 53 (69): 361-5.

Background/AimsNitric oxide (NO) production is elevated in the intestine and may contribute to intestinal injury during inflammation. However, how the expression of inducible NO synthase (iNOS) mRNA and endothelial NO synthase (eNOS) mRNA in the esophageal mucosa contribute to mucosal damage caused by reflux esophagitis remains unknown. Since vascular endothelial growth factor (VEGF) exerts its action on microcirculation, contributing to angiogenesis and inflammation, we examined the role of VEGF together with iNOS and eNOS on development of reflux esophagitis.MethodologyThe mRNA expression levels of iNOS, eNOS and VEGF were measured in biopsy specimens from 25 patients with reflux esophagitis, using TaqMan PCR and reverse transcription PCR.ResultsThe expression of iNOS mRNA in the esophageal mucosa increased parallel to the severity of the esophagitis. There were no significant differences between both eNOS and VEGF mRNA expression levels and the severity of the esophagitis. The existence of gastric mucosal atrophy, hiatus hernia, therapy and Helicobacter pylori infection did not affect the levels of mRNA expression.ConclusionsThe accumulation of NO, produced by iNOS, was considered to be related to the exacerbation of reflux esophagitis. Therapeutic intervention that reduces NO production may thus be of use in preventing development of esophageal mucosal injury in patients with reflux esophagitis.

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