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腹裂患儿肠道损伤的病因学,II. 组织学改变、黏膜功能及收缩性的时间变化与可逆性

Etiology of intestinal damage in gastroschisis, II. Timing and reversibility of histological changes, mucosal function, and contractility.

作者信息

Langer J C, Bell J G, Castillo R O, Crombleholme T M, Longaker M T, Duncan B W, Bradley S M, Finkbeiner W E, Verrier E D, Harrison M R

机构信息

Fetal Treatment Program, University of California, San Francisco.

出版信息

J Pediatr Surg. 1990 Nov;25(11):1122-6. doi: 10.1016/0022-3468(90)90745-u.

Abstract

Previous work in the fetal lamb examined the relative effects of amniotic fluid and bowel constriction in the etiology of bowel damage in gastroschisis. The present study used the same model to assess the timing and reversibility of these changes during gestation. Gastroschisis was created at 80 days' gestation, and a tape was placed around the bowel to cause gradual constriction with growth. Lambs were killed at 100 days, 120 days, and term. Bowel damage was assessed using histology, mucosal enzyme activity, and in vitro motility. In an additional "repaired" group, the constrictor was removed at 120 days, a silastic pouch placed over the bowel, and bowel damage assessed at term. Normal fetuses at each gestational age were used as controls. A fibrous peel was observed at all gestational ages. Mucosal villous atrophy and mesenteric venous and lymphatic dilation were mild at 100 and 120 days, but severe at term. These changes were present but mild in repaired animals at term. Mucosal enzyme activity decreased gradually with gestational age; inhibition of maltase activity was maximal at term, and was significantly reversed by repair, whereas inhibition of aminooligopeptidase activity was maximal at 120 days, and was not affected by repair. Protein/DNA, DNA/weight, and protein/weight ratios showed that repaired mucosal cells were significantly more proliferative, smaller, and less mature than control or gastroschisis cells. In vitro motility studies demonstrated a mild decrease in contractility at 100 and 120 days, and a large decrease at term. This deleterious effect at the end of gestation was only partially reversed by repair in utero.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

先前对胎羊的研究探讨了羊水和肠管狭窄在腹裂肠损伤病因学中的相对作用。本研究使用相同模型评估这些变化在妊娠期的发生时间和可逆性。在妊娠80天时造成腹裂,并在肠管周围放置胶带,使其随生长逐渐狭窄。在妊娠100天、120天和足月时处死羔羊。使用组织学、黏膜酶活性和体外运动性评估肠损伤。在另外一个“修复”组中,在120天时移除收缩器,在肠管上放置一个硅橡胶袋,并在足月时评估肠损伤。各胎龄的正常胎儿用作对照。在所有胎龄均观察到纤维性包膜。100天和120天时黏膜绒毛萎缩以及肠系膜静脉和淋巴管扩张较轻,但足月时严重。这些变化在足月的修复动物中存在但较轻。黏膜酶活性随胎龄逐渐降低;麦芽糖酶活性的抑制在足月时最大,且通过修复显著逆转,而氨基寡肽酶活性的抑制在120天时最大,且不受修复影响。蛋白质/DNA、DNA/体重和蛋白质/体重比率显示,修复后的黏膜细胞比对照或腹裂细胞增殖明显更多、体积更小且成熟度更低。体外运动性研究表明,100天和120天时收缩性轻度降低,足月时大幅降低。妊娠末期的这种有害作用仅通过子宫内修复部分逆转。(摘要截断于250字)

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