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新型腐蚀性损伤兔模型中超薄上消化道内窥镜诱发的食管狭窄

Esophageal stricture induced by an ultraslim upper endoscope in a novel rabbit model of corrosive injury.

作者信息

Hwang Jae Chul, Jin Bohwan, Kim Jang-Hee, Lim Sun Gyo, Yang Min Jae, Kim Soon Sun, Shin Sung Jae, Lee Kee Myung, Kim Jin Hong

机构信息

Department of Gastroenterology, Ajou University School of Medicine , Suwon , Korea.

出版信息

Scand J Gastroenterol. 2014 Jan;49(1):30-4. doi: 10.3109/00365521.2013.848229. Epub 2013 Oct 28.

Abstract

OBJECTIVE

Benign esophageal strictures are regularly encountered problems in clinical practice. The management of refractory benign esophageal stricture, which fails to establish adequate food passage despite multiple dilatation sessions, has been considered challenging. Experimental animal models are essential for the development of effective treatment methods. The aim of this study was to establish a new animal model of benign esophageal stricture using rabbits.

MATERIAL AND METHODS

Corrosive injury of the esophagus was induced by administration of 1 ml of 1.5% sodium hydroxide in eight rabbits using an ultraslim upper endoscope equipped with a 5-Fr polytetrafluoroethylene tube and 5-Fr balloon catheter. Two weeks after corrosive injury, endoscopic examination was performed to confirm the state of the injury site. Four weeks after corrosive injury, the esophageal stricture was assessed by endoscopy and esophagography. All animals were then euthanized.

RESULTS

Two weeks after corrosive injury, endoscopic examination showed that ulceration had been induced. Four weeks after corrosive injury, endoscopic, radiologic and gross examinations showed that esophageal stricture had been induced without complications in all animals. The esophageal lumen diameter was reduced by an average of 51.8% (range, 48.3%-57.2%), and the mean stricture length was 25.7 mm (range, 20.1-29.3 mm). Microscopic examination revealed focal ulceration and submucosal thickening secondary to fibrosis.

CONCLUSIONS

Rabbit esophageal stricture induced by endoscopic delivery of a small amount of low-concentration sodium hydroxide is a relatively simple, safe, and reproducible animal model. This model may be useful in the development of new treatment methods for esophageal stricture.

摘要

目的

良性食管狭窄是临床实践中经常遇到的问题。尽管进行了多次扩张,但仍未能建立足够食物通道的难治性良性食管狭窄的管理被认为具有挑战性。实验动物模型对于有效治疗方法的开发至关重要。本研究的目的是使用兔子建立一种新的良性食管狭窄动物模型。

材料与方法

使用配备5Fr聚四氟乙烯管和5Fr球囊导管的超薄上消化道内窥镜,给8只兔子注射1ml 1.5%氢氧化钠,诱导食管腐蚀性损伤。腐蚀性损伤两周后,进行内窥镜检查以确认损伤部位的状态。腐蚀性损伤四周后,通过内窥镜检查和食管造影评估食管狭窄情况。然后对所有动物实施安乐死。

结果

腐蚀性损伤两周后,内窥镜检查显示已诱发溃疡。腐蚀性损伤四周后,内窥镜、放射学和大体检查显示所有动物均诱发了食管狭窄且无并发症。食管腔直径平均缩小51.8%(范围为48.3%-57.2%),平均狭窄长度为25.7mm(范围为20.1-29.3mm)。显微镜检查显示局灶性溃疡和继发于纤维化的黏膜下增厚。

结论

通过内窥镜输送少量低浓度氢氧化钠诱导的兔食管狭窄是一种相对简单、安全且可重复的动物模型。该模型可能有助于开发食管狭窄的新治疗方法。

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