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羊膜内给予尿胰蛋白酶抑制剂可维持先天性脐膨出胎鸡胚中胎粪诱导的肠损伤的肠收缩性。

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

机构信息

Department of Pediatric Surgery, Dokuz Eylül University, Medical School, Izmir, Turkey.

出版信息

J Pediatr Surg. 2013 Jul;48(7):1495-8. doi: 10.1016/j.jpedsurg.2012.10.002.

Abstract

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.

摘要

背景

先天性脐膨出可导致肠动力障碍。尿胰蛋白酶抑制剂(UTI)已被证明可预防先天性脐膨出鸡胚的肠损伤。但尚未研究宫内给予 UTI 对先天性脐膨出肠动力的影响。

方法

使用 5 日龄受精鸡胚。通过羊膜腔而不打开尿囊腔来创建先天性脐膨出。共有 6 组:对照组、单纯先天性脐膨出组、先天性脐膨出加胎粪组和 3 个治疗组。在治疗组中,分别将 100 IU/mL、200 IU/mL 和 400 IU/mL 的 UTI 注入先天性脐膨出加胎粪鸡胚的羊膜腔中。通过组织病理学测量各组肠浆膜厚度。通过体外器官浴技术评估肠收缩,并将反应表示为乙酰胆碱诱导的最大收缩。

结果

与对照组和单纯先天性脐膨出组相比,先天性脐膨出加胎粪组、100 IU/mL 和 200 IU/mL UTI 组的浆膜厚度显著增加。400 IU/mL UTI 组的浆膜厚度与对照组和单纯先天性脐膨出组相似。先天性脐膨出加胎粪组、100 IU/mL 和 200 IU/mL UTI 组的肠收缩力减弱。对照组、单纯先天性脐膨出组和 400 IU/mL UTI 组之间的收缩力无显著差异。

结论

宫内给予 UTI 可维持先天性脐膨出鸡胚的肠收缩力。然而,在人类先天性脐膨出病例中使用 UTI 来维持肠动力障碍还需要进一步的实验和临床试验。

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