Journal of Pathology and Translational Medicine

Original Article

An Experimental Study of Pathogenesis of Duodenal Ulceration Produced by Mepirizole.: Myung Jae Kang, Jae Ryong Jung, Hye Soo Lee, Sang Ho Kim; Korean J Pathol. 1988;22(4):383-392.

Abstract PDF: To investigate the pathogenesis of the duodenal ulceration produced by mepirizole (1-(4-methoxy-6-methyl-2-pyrimidinyl)-3-methyl-5-methoxypyrazole) in rat, the effects of various concentraion and sorts of antiulcer drugs and truncal vagotomy on the mepirizole (200 mg/kg of body weight) induced duodenal ulcers were observed morphologically, and after mepirizole administration (200 mg/kg), amount and acidity of gastric jucie were measured sequently. The results were as follows: 1) In the control group of fasting for 24 hours after mepirizole administration only, duodenal ulcers were developed in all animals with 21.5+/-5.8 mm2 of ulcer index, perforation rate was 15%, and mortality rate was 0%. But lesions of the stomach were hemorrhagic and erosive with erosion index of 3.8+/-1.6 mm2. 2) The antiulcer drugs were significantly inhibited duodenal ulceration and gastric erosion produced by mepirizole although the inhibition effects were different. 3) After truncal vagotomy, duodenal ulcer and gastric erosion induced by mepirizole were also significantly inhibited. 4) On the gastric analysis, decrease of amount, increase of acidity, and decrease of concentration of gastric juice were observed after administration of mepirizole compared with nontreated normal group. Above findings suggest that the pathogenesis of the duodenal ulceration by mepirizole is the action of gastric acid on the duodenal mucosa with breakdown of defence mechanisms of the duodenum.

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