Intra-amniotic administration of urinary trypsin inhibitor preserves intestinal contractility in meconium induced intestinal damage in chick embryos with gastroschisis

Background: Intestinal damage causes intestinal dysmotility in gastroschisis. Urinary trypsin inhibitor (UTI) has been shown to prevent intestinal damage in chick embryos with gastroschisis. The effect of intra-amniotic administration of UTI on intestinal motility in gastroschisis has not been investigated.

Methods: Five-day-old fertilized chick embryos were used. Gastroschisis was created through the amniotic cavity without opening the allantoic cavity. There were six groups; control, gastroschisis only, gastroschisis plus meconium and three treatment groups. In the treatment groups, 100 IU/mL, 200 IU/mL and 400 IU/mL UTI were instilled into the amniotic cavity of the gastroschisis plus meconium embryos, respectively. Serosal thickness of the intestines in each group was measured histopathologically. The contractions of the intestines were evaluated by in vitro organ bath technique and the responses were expressed as maximal contraction induced by acetylcholine.

Results: The serosal thickness was significantly increased in the gastroschisis plus meconium, 100 IU/mL, 200 IU/mL UTI groups compared to control and gastroschisis only groups. The serosal thickness of the 400 IU/mL UTI group was similar to control and gastroschisis only groups. Contractility of the intestines was diminished in the gastroschisis plus meconium, 100 IU/mL and 200 IU/mL UTI groups. There was no significant difference regarding contractility among control, gastroschisis only and 400 IU/mL UTI groups.

Conclusion: Intra-amniotic administration of UTI preserves intestinal contractility in chick embryos with gastroschisis. However, preservation of intestinal dysmotility by using UTI in the human gastroschisis cases needs further experimental and clinical trials.