de Lagausie P, Guibourdenche J, de Buis A, Peuchmaur M, Oury J F, Aigrain Y, Sibony O, Luton D
Département de périnatologie, Hôpital Robert Debré, Paris, France.
J Pediatr Surg. 2002 Aug;37(8):1160-4. doi: 10.1053/jpsu.2002.34463.
BACKGROUND/PURPOSE: 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.
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.
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.
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.
背景/目的：最近，作者发现患有腹裂的人类胎儿存在羊水炎症反应，而旨在打破炎症循环的羊水置换似乎对结局有有利影响。因此，作者在胎羊中设计了一种腹裂模型，其中羊膜腔灌注显著改善了有害过程。他们推测羊水反流和消化酶的存在会引发并维持炎症过程。
为了验证这一假设，作者使用了他们的胎羊腹裂模型并结合食管结扎，将其与接受或未接受羊膜腔灌注的腹裂模型进行比较。
在妊娠中期（第70至80天）接受手术的34只胎儿中，11只在子宫内死亡或死产，8只患有腹裂并接受羊膜腔灌注，8只患有腹裂但未接受羊膜腔灌注，7只患有腹裂并进行食管结扎。另有9只对照胎儿。在第145天通过剖宫产将胎儿处死。对带有纤维包膜的腹外肠管进行组织学检查。对照组肠肌层厚度（微米）为82.7±19，未接受羊膜腔灌注的胎儿为159±56，接受羊膜腔灌注的胎儿为126±21（P = 0.001），食管结扎合并腹裂的胎儿为240±225.8。浆液性纤维化厚度和浆细胞浸润也得到了相同的结果。羊水铁蛋白、脂肪酶和蛋白质检测显示，只有羊膜腔灌注将铁蛋白和蛋白质水平降至与对照组相似的水平，从而说明了其对炎症的预防作用，并且食管结扎并不能防止消化酶存在于羊水中。
在这个胎羊腹裂模型中，食管结扎本应通过防止消化酶经口反流并形成相对羊水过多来保护外露肠管，但并未改善炎症和有害过程，而羊膜腔灌注对其预防效果最佳。
