Abstract
Background. The relationship between Hipylori (Hpj-colonization and the formation of stress-induced gastric mucosal injury has remained unknown. In the Hp-infected gastric mucosa, urease-dependent ammonia (NH3) production is reportedly important to induce gastric lesions. The present study was designed to investigate whether NHrpretreatment enhances the formation of gastric lesion in response to emotional stress. Method. Twelve CS7BL/6 mice were treated with 0.01%-NH3 through the gastric tube once a day for a week before applying emotional stress, and other II mice were treated with distilled water. To provide emotional stress, the communication box paradigm, in which each mouse (responder) was placed in transparent plastic compartment adjacent to mice receiving electrical stimulation (3 hours (19:30-22:30) per day for 3 days; sender), was used. After the overnight fasting, the stomach of each animal was examined. Macroscopic and microscopic evaluation were performed in each stomach. Mucosal activity of myeloperoxidase (MPO), an index of neutrophil accumulation, as well as the contents of thiobarbitulate reactive substances (TBARS), an index of mucosal lipid peroxidation were measured (Free Radie. Bioi. Med. 26:679, 1999). Results. The responder mice pretreated with 0.01%-NH3 (NH3-responder) developed more severe gastric lesions than those pretreated with distilled water (control-responder). MPO activity was enhanced in NH3-responder (0.72±0.3S mU/mg protein) more than that in the control-responder (0.3S±0.09 mU/mg protein) (p<O.OS). TBARS contents further increased in NH3-responder (4.84± 1.36 nmol/mg protein) compared with those in the control-responder (2.2S±0.6S nmol/mg protein) (p<O.OS). Luminol-dependent chemiluminescence (compatible to neutrophil-derived OCn was higher in NHrresponder (S.22±0.S4 countsl mg) than that in the control-responder (2.76± 1.S0 counts/mg). Conclusion. Intragastric ammonia overloading such as Hp-colonization could enhance gastric mucosal lesion in response to emotional stress. This injury may be associated with an enhanced production of oxygen free radicals from accumulated neutrophils.
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