암모니아로 인한 위점막 손상의 연구 - Helicobacter pylori의 위장질환 발생기전과 관련하여 = Ammonia Induced Gastric Mucosal Injury : Role of Ammonia in the Mechanism of Helicobacter pylori-related Gastric Disease암모니아로 인한 위점막 손상의 연구 - Helicobacter pylori의 위장질환 발생기전과 관련하여

다국어 초록 (Multilingual Abstract)

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다국어 초록 (Multilingual Abstract)

Background/Aims: After the identification of Helicobacter pylori as a major cause of gastro- duodenal diseases, special attention was paid to elucidating the mechanism of tissue injury and mucosal inflammation. Among the many exotoxins of H.pylori, ammonia was considered to be a resistant factor against the acidic condition, and to be a pathogenic factor causing mucosal injury. We studied the pathogenesis of the ammonia induced gastric mucosal injury. Methods: We perforrned biochemical and pathological experiments in male Sprague Dawley rats(N=51, 200+ 30gm). The rats were fasted and were killed at 2, 10, and 30 minutes following administration of lml of ammonia(A2, A10, A30, N=6 respectively), or 75% ethanol(E2, E10, E30, N=5, respectively). Additional groups of rats sacrificed on the 8th day following daily administration of 1ml of 1% ammonia(AC, N=6) or 75% ethanol (EC, N=6). After death, some portion of the stomach was rapidly homogenized and processed for the determination of sulphydryls, glutathione(GSH), and malondialdehyde(MDA). Additionally some portion of the stomach was examined pathogically. Results: GSH(p mol/gm tissue) in the rat's gastric mucosa changed from 2.4+0.4 in controls to 1.0+0.3, 0.5+0.1, 0.5+O.l, 0.6+0.1, or 1.4+0.2, 0.4+0.1, 0.5+0.1, and 0.6+0.2 in A2, A10, A30, AC, or E2, E10, E30, and EC, respectively. The level of GSH was significantly decreased(P<0.01) in A2 compared to E2. Also MDA(nmol/gm tissue) in the rats gastric mucosa changed from 26.3+4.4 in controls to 75.7+25.8, 59.9+13.1, 47.6+11.1, 69.2+ 25.3, or 46.3+18.1, 63.6+23.9, 46.8+20.0, and 71.9+20.9 in A2, A10, A30, AC, or E2, E10, E30, and EC, respectively. MDA was significantly increased(P<0.01) in A2 compared to E2. The gastric mucosa in A2 showed more severe hemorrhage and ischemia than E2(50Fo, 30% of the stomach in A2, VS 30%, 0% of the stotnach in E2,) Conclusions: The depletion of the mucosal sulphydryls, GSH, the release of free radicals, and early vascular injury are considered to play an important role in the pathogenesis of ammonia and H.pylori induced gastric injury, and ammonia was found to be more damaging in the rats stomach than ethanol in the early stage of injury. (Korean J Gastroenterol 1997; 29:442-448)