食管良性狭窄球囊导管扩张术后再狭窄病理机制的实验研究

目的　探讨食管良性狭窄球囊导管扩张术后食管再狭窄的发生机制。方法　采用双球囊导管法制作大鼠食管良性狭窄模型 (对照组 ) ;使用PTCA球囊导管对食管良性狭窄进行扩张制作食管再狭窄模型 (实验组 )。大鼠食管狭窄和再狭窄形成过程中的定量指标采用图像分析仪测量、定性指标采用免疫组织化学方法观察。结果　成功制作大鼠食管良性狭窄和再狭窄模型 49个。实验组术后食管黏膜层、肌层及全层的载面积和周长都有明显增加 ,与对照组比较统计学上有意义 (P <0 .0 5 )。实验组术后第 5天 ,增殖细胞核抗原 (PCNA)开始表达 ,持续到 1个月仍有表达。术后第 1天 ,纤维连接蛋白(FN)就开始表达 ;第 2 1天 ,FN表达仍呈阳性 ;第 30天时 ,FN仍有部分呈强阳性表达。结论　食管良性狭窄球囊导管扩张术后再狭窄的主要原因之一是PCNA和FN持续的过度分泌

Experimental study of the mechanism in esophageal restenosis after balloon dilation of benign stricture

Objective Experimental study of the mechanism in esophageal restenosis after balloon dilation of benign stricture.Methods Esophageal stenosis model of the rats was created by 5ml of 50% NaOH solution burn with double balloon method, and esophageal restenosis (RS) model was developed by esophageal stenosis with dilation of PTCA balloon catheter. Quantitative and quanlitative analysis of esophageal stenosis and RS formation in the rats were observed and recorded by analytic measurements imaging and immunohistologic chemistry respectively. Results Esophageal benign stricture and RS model of 49 rats were developed. Cross section area and perimeter of esophageal mucosa layer, muscule layer and the whole layer had increased in experimental group. Comparing to control group, it had remarkable significance in statistics ( P <0.05). PCNA was expressed in 5th day after dilation, and persisted to 1st month. FN was expressed in the 1st day after dilation, still positive on 2lst days, partly strong on 30th day. Conclusions The continued over secretion at all stage of PCNA and FN plays an important role in the RS after balloon dilation of esophageal benign stenosis.