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Experimental small bowel obstruction in chick embryos: Effects on the developing enteric nervous system
Robert A Schoenberg1, Dietrich Kluth
1Hamburg, Germany.
Insights
Experimentally induced small bowel atresias in chick embryos caused significant changes to the enteric nervous system (ENS). These structural alterations in the ENS likely explain post-surgical motility disorders in infants with similar conditions.
Area of Science:
- Developmental biology
- Neuroscience
- Gastroenterology
Background:
- Congenital small bowel atresias often lead to intestinal motility disorders post-surgical repair.
- These motility issues may stem from alterations in the enteric nervous system (ENS) due to intestinal obstruction.
Purpose of the Study:
- To investigate the structural changes in the ENS following experimentally induced small bowel atresias in chick embryos.
- To correlate these ENS changes with potential causes of motility disorders observed after surgical repair of intestinal atresias.
Main Methods:
- Small bowel atresias were surgically induced in 90 chicken embryos on day 11 via microsurgical ligation.
- Histological analysis included silver-staining, semithin serial sections, transmission electron microscopy, and acetylcholinesterase (AChE) staining.
- Normal chick embryos of the same age served as controls for comparison.
Main Results:
- Experimentally induced atresias mimicked human congenital small bowel atresias macroscopically.
- Microscopically, the submucosal plexus was nearly absent both proximally and distally to the obstruction.
- The myenteric plexus was reduced in the proximal dilated segment, with disrupted axonal nets and altered ganglion cell clustering. Cells of Cajal were absent.
Conclusions:
- Structural changes in the ENS were observed secondary to experimentally induced small bowel atresias.
- Proximal gut dilatation, not ischemia, appears to be the primary driver of these ENS alterations.
- These findings provide a potential explanation for motility disorders following surgical repair of intestinal atresias, anorectal malformations, and Hirschsprung's disease.
Background/Purpose:
After surgical repair of congenital small bowel atresias, intestinal motility disorders often are observed. These may be caused by changes in the enteric nervous system (ENS) secondary to obstruction. To assess these changes, small bowel atresias were induced experimentally in chick embryos.
Methods:
On day 11, the small intestines of 90 chicken embryos were ligated microsurgically in ovo. Breeding of the eggs was continued until day 19. The small bowel was removed, fixed, and embedded for silver-staining, semithin serial sections, and transmission electron microscopy. Additionally, acetyl-cholinesterase (AChE)-staining was performed. Normal chick embryos of the same age served as controls.
Results:
Macroscopically, experimentally induced small bowel atresias had the same characteristics as human newborns. Microscopically, the wall structure was preserved; however, the ENS differed markedly from controls. Both proximal and distal to the obstruction, the submucosal plexus was almost completely absent, whereas the myententeric plexus was diminished only in the proximal dilated blind pouch. The axonal net was disrupted additionally. Ganglion cells of the myenteric plexus in the proximal segment were arranged in longitudinal clusters of densely packed cells. In the distal segment ganglion cells formed round clusters. The cells of Cajal, which normally surround the myenteric ganglia, were absent in the proximal and distal segments.
Conclusions:
In our experiments, structural changes in the ENS could be observed secondary to experimentally induced small bowel atresias in the chick. Because of the lack of ischemia in this model, the main cause of these ENS changes seems to be the dilatation oft the proximal gut. Dilatations are common features in intestinal atresias, anorectal malformations, and Hirschsprung's disease. Our observations, thus, explain motility disorders after the surgical repair of these diseases.