title: A possible defensive mechanism in the basal region of gastric mucosa and the healing of erosions.
abstract: A possible defensive mechanism in the basal region of the gastric mucosa was hypothesized in the present study. In vivo microscopy was performed to observe the basal region after thermal injury to the back skin of rats. A donor of nitric oxide, 3-morpholinosydnonimine hydrochloride (SIN-1), or a serine protease inhibitor, camostat mesilate, was administered. Anti-vascular endothelial growth factor (VEGF) neutralizing antibody was administered 5 hours after thermal injury (anti-VEGF group). Post-capillary venules could be observed in the basal region of the gastric mucosa (PV-BGM). The PV-BGM was dilated 5 hours after thermal injury, and it was reduced by the administration of SIN-1 or pre-treatment with camostat mesilate. In the control group, the erosions did not reach the basal region of the gastric mucosa. Most of the erosions healed within 72 hours. Delayed healing was observed in the anti-VEGF group. In this group, exudation and congestion in the basal region were observed at 24 hours, and ulcer formation was observed at 72 hours after thermal injury. It is thus hypothesized that blood flow of the PV-BGM increases when superficial mucosal circulation is disturbed. The PV-BGM can contribute to defensive mechanisms in the basal region of gastric mucosa. The abnormal healing process may disturb the defensive mechanism at the base of the gastric mucosa, thereby resulting in ulcer formation.
authors.affiliation: Department of Surgery, Keio University School of Medicine, Tokyo, Japan. masashi@sc.itc.keio.ac.jp
authors.forename: Masashi
authors.initials: M
authors.lastname: Yoshida
authors.forename: Go
authors.initials: G
authors.lastname: Wakabayashi
authors.forename: Hideki
authors.initials: H
authors.lastname: Ishikawa
authors.forename: Kaori
authors.initials: K
authors.lastname: Kameyama
authors.forename: Motohide
authors.initials: M
authors.lastname: Shimazu
authors.forename: Minoru
authors.initials: M
authors.lastname: Tanabe
authors.forename: Shigeyuki
authors.initials: S
authors.lastname: Kawachi
authors.forename: Koichiro
authors.initials: K
authors.lastname: Kumai
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Kubota
authors.forename: Yoshihide
authors.initials: Y
authors.lastname: Otani
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Saikawa
authors.forename: Katsuko
authors.initials: K
authors.lastname: Sano
authors.forename: Masaki
authors.initials: M
authors.lastname: Kitajima
mesh_terms: D000818:Animals; D002056:Burns / Q000150:complications; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004952:Esters; D005122:Exudates and Transudates / Q000378:metabolism; D016670:Gabexate / Q000031:analogs & derivatives* / Q000494:pharmacology; D005753:Gastric Mucosa / Q000098:blood supply / Q000503:physiopathology*; D006146:Guanidines; D008297:Male; D008833:Microcirculation; D008981:Molsidomine / Q000031:analogs & derivatives / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012867:Skin / Q000293:injuries; D013276:Stomach Ulcer / Q000209:etiology / Q000503:physiopathology*; D013312:Stress, Physiological / Q000150:complications; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors / Q000502:physiology; D014699:Venules / Q000503:physiopathology
chemical_list: D004791:Enzyme Inhibitors; D004952:Esters; D006146:Guanidines; D020030:Nitric Oxide Donors; D042461:Vascular Endothelial Growth Factor A; C034532:camostat; D009569:Nitric Oxide; D016670:Gabexate; C002385:linsidomine; D008981:Molsidomine