Suppr超能文献

通过在兔子身上用酸和胃蛋白酶诱导实验性食管炎,模拟人类反流性食管炎。

Experimental esophagitis induced by acid and pepsin in rabbits mimicking human reflux esophagitis.

作者信息

Lanas A, Royo Y, Ortego J, Molina M, Sáinz R

机构信息

Services of Gastroenterology, Research Unit (Unidad Mixta de Investigación),University Hospital and University of Zaragoza, Spain.

出版信息

Gastroenterology. 1999 Jan;116(1):97-107. doi: 10.1016/s0016-5085(99)70233-7.

Abstract

BACKGROUND & AIMS: The lack of appropriate animal models might explain the paucity of information on the mechanisms of mucosal damage and defense in reflux esophagitis. The aim of this study was to develop a model of esophagitis in rabbits mimicking human reflux esophagitis.

METHODS

New Zealand white rabbits underwent surgery for placement of a plastic tube into the cervical esophagus. Acidified pepsin (AP) was intermittently perfused for different periods. Esophageal injury was assessed by macroscopic and microscopic examination, including the cell proliferation immunohistochemical parameter mib1.

RESULTS

Rabbit losses (20%) were attributable mostly to postsurgical mortality and tube displacement. Perfusion of AP for 60 min/12 h or 45 min/12 h induced high-grade esophagitis by days 3 and 5, respectively, characterized by diffuse erosion/ulceration, inflammation, bleeding, and reactive epithelial changes. Perfusion of acidified pepsin for 60 min/day, especially at 30 min/12 h, induced low-grade esophagitis characterized by superficial epithelial loss, mild/absent inflammation, and epithelial reactive changes including increased cell proliferation, basal hyperplasia, and papillomatosis, which reached maximal expression by day 7. This perfusion regimen induced mucosal adaptation to damage.

CONCLUSIONS

Different and highly reproducible esophageal mucosal lesions mimicking human reflux esophagitis can be induced in rabbits with repetitive acid and pepsin exposure.

摘要

背景与目的

缺乏合适的动物模型可能解释了反流性食管炎黏膜损伤和防御机制方面信息匮乏的原因。本研究的目的是建立一种模仿人类反流性食管炎的兔食管炎模型。

方法

对新西兰白兔进行手术,将塑料管置入颈段食管。不同时间段间歇性灌注酸化胃蛋白酶(AP)。通过宏观和微观检查评估食管损伤,包括细胞增殖免疫组化参数mib1。

结果

兔的损失(20%)主要归因于术后死亡和导管移位。分别在第3天和第5天,AP灌注60分钟/12小时或45分钟/12小时可诱发重度食管炎,其特征为弥漫性糜烂/溃疡、炎症、出血和反应性上皮改变。酸化胃蛋白酶每天灌注60分钟,尤其是30分钟/12小时,可诱发轻度食管炎,其特征为浅表上皮脱落、轻度/无炎症以及上皮反应性改变,包括细胞增殖增加、基底增生和乳头瘤样病变,这些改变在第7天达到最大程度表达。这种灌注方案可诱导黏膜对损伤产生适应性变化。

结论

通过反复给予酸和胃蛋白酶,可在兔身上诱发不同且高度可重复的模仿人类反流性食管炎的食管黏膜病变。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验