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Updated: Aug 16, 2026
A Mouse Model of Intestinal Partial Obstruction
Published on: March 5, 2018
Natural history of experimental intestinal atresia: morphologic and ultrastructural study
S M Baglaj1, J Czernik, J Kuryszko
1Department of Paediatric Surgery, Wroclaw University of Medicine, Wroclaw, Poland.
Insights
This study reveals that induced intestinal atresia (IA) in chick embryos causes progressive bowel damage, but adaptive mechanisms can partially restore intestinal structure later in development.
Area of Science:
- Developmental biology
- Gastroenterology
- Pathology
Background:
- Congenital intestinal atresia (IA) is a significant cause of neonatal bowel obstruction.
- Understanding the natural history of IA is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the natural history of surgically induced intestinal atresia (IA) in chick embryos.
- To characterize the macroscopic, histologic, and ultrastructural changes in the developing intestine following IA induction.
Main Methods:
- Intestinal atresia (IA) was induced in chick embryos on day 12 of incubation via mesenteric vessel electrocoagulation.
- Macroscopic, light microscopy, and electron microscopy (scanning and transmission) were used to examine bowel changes.
- Investigations were conducted on experimental, control, and sham-operated groups at multiple incubation stages (days 15, 17, 19, 21).
Main Results:
- A high success rate (96%) of IA induction was achieved, with 81% developing Type II (cord) atresia.
- Progressive necrosis, mucosal thinning, and epithelial changes were observed, with initial rapid progression followed by slower changes.
- Ultrastructural analysis revealed enterocyte flattening and microvilli atrophy, with surprising signs of adaptive repair by days 19-21.
Conclusions:
- The histologic and ultrastructural lesions in experimental IA are dynamic and not solely due to intraluminal pressure.
- The chick embryo model provides insights into the complex pathogenesis and potential for adaptation in intestinal atresia.
Purpose:
The aim of this study was to evaluate a natural history of congenital intestinal atresia (IA) in the chick embryo and to assess the type and nature of changes in the intestine at various developmental stages.
Methods:
Chick embryos underwent operative induction of IA on the 12th day of incubation. The procedure consisted of electrocoagulation of the mesenteric vessels supplying a 7- to 8-mm intestinal segment. The embryos were subjected to macroscopic examination, histologic and ultrastructural studies of the preatretic and postatretic bowel using the light microscope, scanning, and transmission electron microscopes. All investigations were performed in an experimental group (operated embryos), in a control group, and in a sham-operated group on the 15th, 17th, 19th, and 21st day of incubation.
Results:
The original technique of an iatrogenic "vascular event" proved to be effective because IA developed in 96% of embryos surviving the procedure. The affected portion of the bowel underwent progressive necrosis, and signs of bowel obstruction could be observed 48 hours after operation. Cord atresia (type II) developed in 81% of embryos. Histologic investigations showed progressive thinning of mucosa, flattening of mucosal folds, and epithelial detachment within the intestine proximal to atresia. There was only mild hypertrophy of the muscular layers. All these pathomorphologic changes were of rapidly progressive nature until the 17th day of incubation. Later, the rate of distension of preatretic bowel and histologic changes were less. Ultrastructural investigation of the proximal bowel showed progressive flattening of the enterocytes associated with their apical bulging, widening of the intercellular spaces, and microvilli atrophy. Surprisingly, at days 19 and 21 of incubation, signs of induction of adaptive mechanisms with partial restoration of near-normal microvilli pattern were observed.
Conclusions:
Study of natural history of experimental IA indicates that histologic and ultrastructural lesions of the bowel are of dynamic nature and are not only the effect of pathologic intraluminal pressure.
