Published online Nov 15, 2003. doi: 10.3748/wjg.v9.i11.2605
Revised: May 23, 2003
Accepted: June 2, 2003
Published online: November 15, 2003
AIM: To elucidate the mechanism of restenosis following balloon dilation of benign esophageal stenosis.
METHODS: A total of 49 rats with esophageal stenosis were induced in 70 rats using 5 mL of 50% sodium hydroxide solution and the double-balloon method, and an esophageal restenosis (RS) model was developed by esophageal stenosis using dilation of a percutaneous transluminal coronary angioplasty (PTCA) balloon catheter. These 49 rats were divided into two groups: rats with benign esophageal stricture caused by chemical burn only (control group, n = 21) and rats with their esophageal stricture treated with balloon catheter dilation (experimental group, n = 28). Imaging analysis and immunohistochemistry were used for both quantitative and qualitative analyses of esophageal stenosis and RS formation in the rats, respectively.
RESULTS: Cross-sectional areas and perimeters of the esophageal mucosa layer, muscle layer, and the entire esophageal layers increased significantly in the experimental group compared with the control group. Proliferating cell nuclear antigen (PCNA) was expressed on the 5th day after dilation, and was still present at 1 mo. Fibronectin (FN) was expressed on the 1st day after dilation, and was still present at 1 month.
CONCLUSION: Expression of PCNA and FN plays an important role in RS after balloon dilation of benign esophageal stenosis.