Notochord-gut failure of detachment and intestinal atresia
Notochord-gut failure of detachment and intestinal atresia
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DOI：
10.1007/s00383-004-1172-0
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发表时间：
2004-06-01
影响因子：
1.8
通讯作者：
Merei, JM
中科院分区：
文献类型：
--
作者：
Merei, JM
在阿霉素治疗的模型中描述了一系列先天性异常，具有人类模式的共同特征。多发性肠闭锁是25%的足月实验大鼠胎仔中发生的这一谱系的一部分。本研究的目的是探讨导致肠闭锁的潜在发育机制。在妊娠第6-9天，以2 mg/kg的剂量对初次定时妊娠的Sprague-Dawley大鼠i. p.注射阿霉素。在器官发生过程中的不同妊娠日取出胚胎，进行连续的横向组织切片检查，并与对照标本进行比较。在实验胚胎中，后肠闭锁见于12天胚胎。肠与脊索的附着是明显的观察结果，导致肠的位置异常。在某些标本中，闭锁的肠分裂背主动脉，甚至位于背主动脉后面。结论：在阿霉素-动物模型中，在器官形成初期，脊索-肠脱离失败导致肠闭锁。可能的潜在机制是挤压一些内胚层细胞以及干扰正常的肠循环导致缺血性坏死。
A spectrum of congenital anomalies have been described in an adriamycin-treated model with common features to the human pattern. Multiple intestinal atresias was part of this spectrum occurring in 25% of full-term experimental rat fetuses. The aim of this study was to examine the underlying developmental mechanism that results in intestinal atresia. Virgin timed-pregnant Sprague-Dawley rats were injected with Adriamycin i.p. at a dose of 2 mg/kg on days 6-9 of gestation. Embryos were removed on different gestational days during organogenesis and serial transverse histologic sections were examined and compared with control specimens. In experimental embryos, hindgut atresia was seen in day 12 embryos. Attachment of the intestine with the notochord was obvious observation resulting in abnormal position of the intestine. In some specimens the atretic intestine was splitting the dorsal aorta or even located behind the dorsal aorta. It is concluded that in the adriamycin-animal model, notochord-intestinal failure of detachment resulted in intestinal atresia during the beginning of organogenesis period. The possible underlying mechanisms are pinching of some endodermal cells as well as interference with normal intestinal circulation resulting in ischemic necrosis.