Alterations of enteric nerve plexus in experimental gastroschisis: is there a delay in the maturation?

BACKGROUND/
PURPOSE: After surgical correction of gastroschisis, intestinal transitory hypoperistalsis usually occurs. Long-term parenteral nutrition often is necessary leading to a higher morbidity associated with this malformation. The etiology of this transitory intestinal hypomotility is unknown. It may be caused by a reversible inflammatory process in the intestinal wall or other causes, including an alteration of the maturation of intestinal neural plexus, because the disturbance disappears spontaneously after a variable period. The aim of this work was to study the neuronal cells of the myenteric plexus of the fetal intestine in experimental gastroschisis. The main hypothesis was that the transitory intestinal dismotility seen in gastroschisis could be secondary to alteration in the maturation of the enteric nervous plexus.
METHODS: Twenty-seven time-mated rabbits, on gestational day 25, were submitted to a midline laparotomy; the gravid bicornuate uterus was exposed and opened, and the more distal fetuses relative to the vaginal opening had the abdominal wall opened by a small incision to produce gastroschisis (n = 29). The fetuses not submitted to gastroschisis were used as controls (n = 12). The amniotic fluid was carefully aspirated from the opened uterus and saved for later repositions. On gestational day 30, the does were again submitted to general anesthesia, and the fetuses were delivered by cesarean section. The fetal intestine was removed, the adjacent mesentery excised, and intestinal specimens were harvested for histologic studies. The specimens were stained for acetyl-cholinesterase activity (AChE) to assess the maturity of the nervous enteric cells and for lactate dehydrogenase (LDH) that identify specifically immature nervous cells. The histologic sections stained by LDH were submitted to histomorphometric analysis of the nervous cells through an image system analysis (Kontron 300). The results were submitted to statistical analyses (P <.05).
RESULTS: Macroscopic alterations of the fetal gastroschisis intestine are similar to the human findings: shortening of the intestine, intestinal wall thickening, and a hypertrophied muscular layer. In the gastroschisis group, histologic AChE activity was decreased in comparison with control intestines. The histomorphometric assessment in slices stained with LDH, which identify immature nervous cells, showed that the neuronal intestinal cells of the gastroschisis group were significantly smaller and more numerous relative to the control group.
CONCLUSIONS: There were significant differences in the nervous plexus of the intestine of fetuses with gastroschisis relative to the controls. The observed morphologic changes may be caused by alteration in the maturation of the intestinal neuronal in gastroschisis. This alteration may explain the transitory intestinal hypomotility observed in infants after surgical correction of gastroschisis.