林爱军,郭启勇,乞文旭,卢再鸣,刘兆玉.实验犬气管狭窄模型留置覆膜、非覆膜金属支架后管腔再狭窄的规律[J].中国医学影像技术,2010,26(9):1648~1651
实验犬气管狭窄模型留置覆膜、非覆膜金属支架后管腔再狭窄的规律
Rule of restenosis after placement of covered and uncovered metal stent in tracheal stricture model: An experimental study in dogs
投稿时间:2010-04-07  修订日期:2010-05-03
DOI:
中文关键词:  气管疾病  狭窄,病理学  支架  动物实验
英文关键词:Tracheal diseases  Constriction, pathologic  Stents  Animal experimentation
基金项目:
作者单位E-mail
林爱军 中国医科大学附属盛京医院放射科,辽宁 沈阳 110004  
郭启勇 中国医科大学附属盛京医院放射科,辽宁 沈阳 110004 guoqy@sj-hospital.org 
乞文旭 中国医科大学附属盛京医院放射科,辽宁 沈阳 110004  
卢再鸣 中国医科大学附属盛京医院放射科,辽宁 沈阳 110004  
刘兆玉 中国医科大学附属盛京医院放射科,辽宁 沈阳 110004  
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中文摘要:
       目的 观察气管狭窄模型内留置覆膜与非覆膜金属支架后管腔再狭窄规律及差异。方法 16只实验犬通过切除部分气管软骨制作气管狭窄模型,分为A、B组(每组8只)。透视引导下气管狭窄处留置支架,A组留置覆膜镍钛合金支架,B组留置网状镍钛合金裸支架。留置支架后第2、4、8、12周各组分别处死2只实验犬,观察气管壁的病理改变。实验犬处死前行螺旋CT检查,观察支架有无移位、管腔再狭窄的位置及程度,计算狭窄指数,比较A组与B组的差异。结果 16只实验犬均成功制作气管狭窄模型并置入支架。两组支架留置后第4周支架端口出现狭窄,第8、12周支架端口狭窄程度逐渐加重,且B组支架体部也出现狭窄。在相同时间点,A组与B组狭窄指数差异无统计学意义(P>0.05)。狭窄主要由组织增生造成,镜下见淋巴细胞浸润、胶原纤维增生。结论 覆膜支架端口增生组织可引起管腔再狭窄,出现时间及程度与裸支架相近。改进支架端口设计是防止及减轻覆膜支架留置后再狭窄的关键。
英文摘要:
      Objective To observe the rule of restenosis after placement of stent in tracheal stricture model, and to discuss the difference between covered and uncovered self-expanding metallic stent (SEMS). Methods Tracheal stricture model were established with extramucosal resection of cartilaginous arches in 16 dogs, which were divided into A and B group (each n=8). Under the guidance of fluoroscopy, polyurethane covered or uncovered SEMS were placed in the tracheal stricture. At the time of 2 weeks, 4 weeks, 8 weeks and 12 weeks after stent placement, two dogs in each group were examined with CT to observe restenosis status and migration, then were sacrificed for pathologic examination. The restenosis status, migration and pathologic changes in different groups were measured and compared. Stenosis indexes at different time in each group were calculated and compared. Results All tracheal stenosis models and stents placement were successful. In both groups, restenosis appeared at 4 weeks at the end of the stents. At the time of 8 weeks and 12 weeks, restenosis became serious at the end of the stents, and restenosis appeared both end and body of the stents in B group. There was no statistical difference of restenosis indexes between the two groups in the same time (P>0.05). Hyperplasia tissue was mainly consisted of aggregated lymphocytes and collagen formation. Conclusion Excessive tissue hyperplasia at the end of the covered stents may induce restenosis. The restenosis time and degree of stricture of covered stents are similar to those of uncovered stents. Improvement of the design at the end of covered stents may be the key point to prevent restenosis.
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