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目的 应用氯苄烷铵(BAC)建立猫贲门失弛缓症模型,探讨贲门失弛缓症发病机制。方法 24只猫随机分为两组,模型组胃镜下LES处环形注射BAC,对照组注射生理盐水,8周后检测食管动力学变化,并取组织进行HE染色、乙酰胆碱酯酶(AChE)免疫组化染色检查和AChE活力测定。结果 模型组下食管括约肌压力较对照组明显升高(P<0.01),两组食管收缩幅度无显著性差异;组织学检查显示模型组环肌层和纵肌层之间可见炎细胞浸润,对照组正常;对照组可见AChE染色阳性神经节,环肌层和纵肌层可见AChE染色阳性产物,模型组AChE染色阳性产物明显减少(P<0.01);模型组乙酰胆碱酯酶活力与对照组比较明显降低(P<0.01)。结论 肌间神经丛的炎性反应和乙酰胆碱酯酶活力降低是贲门失弛缓症的重要发病原因。
Objective To establish a model of achalasia in cats with benzalkonium chloride (BAC) and explore the pathogenesis of achalasia. Methods Twenty-four cats were randomly divided into two groups. The model group received intragastric injection of BAC at LES, the control group received normal saline, and the esophageal motility was measured after 8 weeks. HE staining and acetylcholinesterase (AChE) Staining test and AChE activity assay. Results The esophageal sphincter pressure in the model group was significantly higher than that in the control group (P <0.01), and there was no significant difference in esophageal contraction amplitude between the two groups. Histological examination showed that inflammatory cells infiltrated between the muscular layer and the longitudinal muscle layer of the model group, The normal group showed normal AChE staining, AChE staining positive products in the muscle and longitudinal muscle of the control group, while the AChE positive products in the model group were significantly decreased (P <0.01). The acetylcholinesterase activity of the model group was more obvious than that of the control group Decreased (P <0.01). Conclusion Myenteric plexus inflammatory response and decreased acetylcholinesterase activity is an important cause of achalasia.