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机构地区:[1]解放军第254医院 [2]天津大学电子信息工程学院
出 处:《解放军医学杂志》2000年第1期47-48,共2页Medical Journal of Chinese People's Liberation Army
摘 要:观察正常犬和形成肝纤维化后犬 2 4h胃内酸环境的变化 ,同时从病理组织学方面观察胃粘膜、血管及分泌腺体等变化。选用杂种犬 1 0只 ,以 CCl4腹腔内注射建立犬纤维化模型。用 Digitrapper MK p H监测仪 ,检测正常犬及注药 1 6周形成肝纤维硬化后 2 4h胃内 p H变化 ,并经组织切片分别观察在正常犬和形成肝硬化后犬胃肠的病理学改变。结果 :2 4h胃内 p H监测 ,在形成肝硬化后比正常犬胃内 p H显著升高 (P<0 .0 1 ) ;病理学显示胃窦、体粘膜有炎细胞浸润 ,粘膜肌及粘膜下纤维组织增生 ,腺体数目减少或腺体萎缩 ,壁细胞数目减少 ,粘膜及粘膜下血管扩张瘀血。结论 :肝硬化后胃内酸度降低 ,可能是导致门脉系统瘀血、缺氧造 - *成壁细胞及腺体数目减少的病理因素 。The changas in gastric acid secretion were observed by 24 hour pH monitoring and the gastric mucosa, blood vessel as well as gastric gland were studied his to pathologic ally before and after repro duction of hepatic cirrhosis. Cirrhosis was successfully reproduced in to dogs by injecting CCl 4 for 16 weeks. The changes in 24 hour gastric pH of all dogs were monitoried by Digitrapper MK Ⅲ before and after cirrhosis. Moreover the stomach and intestinal awalls were studied pathologically. the gastric pH was higher significantly ( P <0.01) after cirrhosis reproduced. There were inflammatory cell infiltration, fibrous tissue proliferation, atrophy or decreasg in number of gastric gland, parietal cell diminution and submucosal angiectasis in the antrum and corpus. Gastric acid was decreased after the produetion of cirrhosis, prubably due to portal congestion and hypoxia, resulting in reduction in the number of parietal cells and gastric glands. Finally it may lead to disturbance in digestive function, congestive gastropathy, and hepatogenic ulcer in the cirrhotic patients.
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