title: Esophageal ligature in experimental gastroschisis.
abstract: OBJECTIVE
  Recently, the authors have shown that in human fetuses suffering from gastroschisis, there is an amniotic fluid inflammatory response and that amniotic fluid exchange designed to disrupt the inflammatory loop seems to have a favorable impact on outcome. The authors, therefore, designed in the fetal sheep a model of gastroschisis in which amnioinfusion significantly improved the deleterious process. They hypothesized that regurgitation and presence of digestive enzyme in the amniotic fluid triggers and maintains the process of inflammation.
  
  
  METHODS
  To test this hypothesis, the authors used their model of gastroschisis in the fetal lamb combined with esophageal ligation and compared it with gastroschisis with or without amnioinfusion.
  
  
  RESULTS
  Of 34 fetuses operated on at midgestation (days 70 through 80), 11 died in utero or were stillborn, 8 had gastroschisis and amnioinfusion, 8 had gastroschisis and no amnioinfusion, and 7 had gastroschisis and esophageal ligation. There were 9 control fetuses. Fetuses were killed at day 145 by cesarean section. Extraabdominal bowels with fibrous peel were processed for histologic examination. Thickness of bowel muscularis (micrometers) was 82.7 +/- 19 for controls, 159 +/- 56 for the nonamnioinfused fetuses, 126 +/- 21 for the amnioinfused fetuses (P =.001), and 240 +/- 225.8 for fetuses with esophageal ligature combined with gastroschisis. The same results were obtained for thickness of serous fibrosis and plasma cell infiltration. Assay of amniotic fluid ferritin, lipase, and protein showed that only amnioinfusion lowered ferritin and protein to levels similar to those of controls, thus, illustrating its preventive effect on inflammation and that esophageal ligature did not prevent digestive enzyme presence in the amniotic fluid.
  
  
  CONCLUSIONS
  In this model of gastroschisis in the fetal sheep, ligature of the esophagus, which was supposed to protect the extruded bowel by preventing oral regurgitation of digestive enzymes and by creating a relative hydramnios, did not improve the inflammatory and deleterious process, which is best prevented by amnioinfusion.
authors.affiliation: Département de périnatologie, Hôpital Robert Debré, Paris, France.
authors.forename: P
authors.initials: P
authors.lastname: de Lagausie
authors.forename: J
authors.initials: J
authors.lastname: Guibourdenche
authors.forename: A
authors.initials: A
authors.lastname: de Buis
authors.forename: M
authors.initials: M
authors.lastname: Peuchmaur
authors.forename: J F
authors.initials: JF
authors.lastname: Oury
authors.forename: Y
authors.initials: Y
authors.lastname: Aigrain
authors.forename: O
authors.initials: O
authors.lastname: Sibony
authors.forename: D
authors.initials: D
authors.lastname: Luton
mesh_terms: D000653:Amniotic Fluid / Q000737:chemistry / Q000201:enzymology*; D000818:Animals; D004195:Disease Models, Animal; D004947:Esophagus; D005293:Ferritins / Q000032:analysis; D020139:Gastroschisis / Q000201:enzymology / Q000209:etiology* / Q000473:pathology*; D007413:Intestinal Mucosa / Q000473:pathology*; D008026:Ligation; D008049:Lipase / Q000032:analysis; D011506:Proteins / Q000032:analysis; D012044:Regression Analysis; D012756:Sheep
chemical_list: D011506:Proteins; D005293:Ferritins; D008049:Lipase