A rat model of autogenous internal arteriovenous fistula and the experimental study on internal fistula stenosis

Objective Intimal hyperplasia at the anastomosis site may cause the failure of autogenous arteriovenous fistula. We designed a rat model to study this process and its mechanism. Methods Wistar rats were subjected to end-to-end anastomosis of the right carotid artery and internal jugular vein. After the operation for 14 and 28 days, rats were sacrificed, and the artery and vein near the anastomosis site were examined for histological changes after staining with HE, combined staining for elastic and collagen fibers, and immunohistochemical staining for PCNA, TGF-β1 and NF-κB. Results After the operation for 14 days, apparent intimal hyperplasia was found at the venous end near the anastomosis site, appearing as polypoid hyperplasia. Vascular smooth muscle cells proliferated with the prominent deposition of collagen fibers. After the operation for 28 days, stenosis of the lumen occurred. The inner elastic layer discontinued at the anastomosis site even after the operation for 28 days. PCNA and NF-κB were highly expressed in medial and adventitial layers of the vein near the anastomosis site after the operation for 14 days and remained highly expressed after 28 days. TGF-β1 was highly expressed in the matrix of adventitial layer. Conclusion This rat model can mimic the local hemodynamic changes in internal fistula. Apparent intimal hyperplasia was seen in this model within 28 days, being useful as an autogenous arteriovenous fistula model. We also found that TGF-β1 and NF-κB were involved in the pathological processes of intimal proliferation in internal fistula.