贲门失弛缓症发病机制的初步探讨

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。

Preliminary study on pathogenesis of achalasia

Objective To elucidate the pathogenesis of achalasia, Benzyldimethyltetradecylammo-nium chloride ( BAC) was used to create amyenteric cat achalasia models. Methods Twenty-four cats were randomized into two groups and injected respectively with BAC in models or saline in controls into the distal esophagus under endoscopy. After 8 weeks, manometry, biopsy with HE stain, acetylcholinesterase activity and immunohistochemistry were studied. Results Manometrically, the pressures of LES in cat models showed higher than those of the controls (P <0. 01) . The esophageal contraction amplitudes were similar in both groups. Histological feature at the LES showed: infiltration of lymphocytes and monocytes between circular and longitudinal muscle layers of models. AChE-positive products and AChE activity have a significant decrease in the BAC-treated models(P <0. 01). Conclusion Inflamation in myenteric nerve plexus and the decrease of AChE activity are the important factors in the pathogenesis of achalasia.