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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 ,这可能是造成肝硬化患者消化功能减退和门脉高压性胃病和相关性溃疡的病理基础
The changes of intragastric acid environment in normal dogs and 24 h after hepatic fibrosis were observed, and the histopathological changes of gastric mucosa, blood vessels and secreting glands were also observed. Ten hybrid dogs were used to establish the model of canine fibrosis by intraperitoneal injection of CCl4. Digitrapper MK p H monitor was used to detect the changes of p H in 24 hours after hepatic fibrosis in normal dogs and 16 weeks after injection. The pathological changes of gastric mucosa in normal dogs and dogs with cirrhosis were observed by histological sections change. Results: 24 h gastric p H monitoring in the formation of liver cirrhosis than normal dogs p H significantly increased (P <0.01); pathological studies showed that the gastric antrum mucosa inflammatory cell infiltration, mucosal muscle and Submucosal fibrosis, glands reduce the number of or glandular atrophy, parietal cells to reduce the number of mucosal and submucosal blood vessels stasis. Conclusion: The decrease of gastric acidity after liver cirrhosis may be the pathological factor leading to portal system blood stasis, hypoxia-making and the number of glandular cells, which may result in the decrease of digestive function and portal hypertension in patients with cirrhosis Gastritis and related pathological basis of ulcer