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[大鼠实验性胎儿生长迟缓时胎盘组织的组织酶学改变]

[Histoenzymologic modifications of placental tissue in experimental fetal hypotrophy in the rat].

作者信息

Tshibangu K, Wilkin P, Thiery M

出版信息

J Gynecol Obstet Biol Reprod (Paris). 1975 Nov-Dec;4(8):1037-53.

PMID:175113
Abstract

Chronic placental vascular insufficiency in the rat was achieved by ligature of the uterine and utero-placental arteries. The fetal and placental hypotrophy observed confirmed the previous observation. However, the placental enzymatic changes showed an increasing gradient of cellular hypoxy from decidua basalis to yolk sac placenta; this gradient is unfavourable to fetuses. The strong depletion of yolk sac enzyme activities demonstrates the reduction of fetomaternal exchanges which are usually predominant in this placental area. The other parts of rat placenta appear relatively less involved in fetal nutrition. Further studies are necessary to understand the changes observed in these activity stainings, such as: oxidoreductases II, acid phosphatase and 5-nucleotidase.

摘要

通过结扎子宫动脉和子宫 - 胎盘动脉造成大鼠慢性胎盘血管功能不全。观察到的胎儿和胎盘萎缩证实了先前的观察结果。然而,胎盘酶变化显示从基底蜕膜到卵黄囊胎盘细胞缺氧呈递增梯度;这种梯度对胎儿不利。卵黄囊酶活性的强烈消耗表明母胎交换减少,而母胎交换通常在该胎盘区域占主导。大鼠胎盘的其他部分似乎较少参与胎儿营养。有必要进一步研究以了解在这些活性染色中观察到的变化,如氧化还原酶II、酸性磷酸酶和5 - 核苷酸酶。

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