Abstract
Gastroesophageal reflux and intestinal distension have been described in survivors
of congenital diaphragmatic hernia (CDH). Deficient enteric innervation demonstrated
in experimental models is a likely explanation for these symptoms. This study aimed
at further characterizing these anomalies and examining esophageal and intestinal
motility in this condition. Pregnant rats received either nitrofen or vehicle on E9.5.
Sections of E15, E18, and E21 esophagus and small bowel were stained for protein gene
product 9.5, nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase (NADPHd),
and acetylcholinesterase (AChE). The proportion of neural tissue/muscle surface was
measured and the NADPHd- and AChE-positive motor endplates (MEPs) were counted. E18
and E21 stomachs were stained for AChE, the ganglia were counted and measured. The
peristalsis of the esophagus and small bowel was video recorded. The relative neural/muscle
surface and the number of NADPHd- and AChE-positive MEPs were decreased on E15 and
E18 in the esophagus and small bowel of embryos with CDH, but they tended to improve
on E21. The number and the mean surface of stomach ganglia were smaller in E18 and
E21 fetuses with CDH. Peristaltic movements were decreased in the esophagus and small
bowel of animals with CDH. Deficient enteric innervation impaired gastrointestinal
motility in experimental CDH. This could explain some long-term morbidity in the human
condition.
Keywords
diaphragmatic hernia - enteric nervous system - peristalsis
