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Abstract :
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.
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