Fetal gastrointestinal motility in a rabbit model of gastroschisis

Gastrointestinal (GI) dysmotility occurs frequently in full-term infants with gastroschisis (GS). Although controversial, preterm delivery of infants with GS has been advocated to prevent the development of GI dysmotility, and understanding the etiology of gestational-related bowel injury may lead to prenatal therapies. Using a fetal rabbit model, the authors assessed in vivo and in vitro GI motility in preterm GS fetuses.

On gestation day 24 (term, 31), surgery was performed in maternal rabbits and GS induced in fetuses, whereas control fetuses underwent sham procedures. On gestation day 29, both groups of fetuses received ultrasound-guided intragastric injection of fluorescein and colored microspheres. Two hours after injection, fetuses were delivered by cesarean section and stomach and small intestine harvested intact. "GI motility" was calculated as the distance traveled by fluorescein divided by total length. In vitro studies of fetal gastric muscle strips contractility responses to bethanechol, a cholinergic agonist, were assessed in an organ bath system. Data were analyzed as paired and unpaired t tests and expressed as means +/- SEM.

GS reduced fetal body weight and intestinal length compared with controls (28.4 +/- 1.4 v. 33.5 +/- 1.5 g, 36.9 +/- 1.8 v. 25.9 +/- 1.2 cm; P <.05, respectively). Fetuses with GS showed markedly reduced in vivo GI motility (51.4 +/- 2.9 v 24.8 +/- 2.7%; P <.05) and in vitro gastric contractile tension (769 +/- 53 v 396 +/- 26 mNcm2; P <.05).

GI exposure to amniotic fluid reduces intestinal motility and gastric contractility functions in the preterm rabbit fetus. The results suggest that GS-associated impairment of GI neuromuscular functions occurs in utero, before term, and may be responsive to manipulation of amniotic fluid content or other therapeutic interventions.