Ultrastructural studies on the placentae of streptozotocin induced maternal diabetes in the rat.

R Padmanabhan, A G al-Zuhair
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Abstract

Following induction of diabetes by a single injection of (IP) streptozotocin (STZ) to pregnant Wistar rats on days 2, 4 and 6 to 12 of gestation, fetuses and placentae were collected on day 20. The controls were either untreated or vehicle treated; alternatively following STZ injection, 2-6 IU of insulin was administered (sc) daily until term. The placentae were fixed in a glutaraldehyde and paraformaldehyde mixture and ultrathin sections were examined under the electron microscope. The structure of the vehicle treated control resembled that of the untreated control. The insulin control group had pathological changes similar to those of the diabetic group but with considerably less frequency. The giant cells in the basal zone of STZ group were numerous; they had abundant dilated cisternae of rough endoplasmic reticulum, intracytoplasmic fibrinoid and nuclear inclusions. The trophospongial cells presented numerous clear vacuoles, lysosomes and myelin bodies. Enlarged vacuoles often impinged deeply on the nucleus. The glycogen cells disintegrated resulting in cyst formation. In the labyrinthine zone, layer I trophoblast revealed increased number of large pores through which layer II trophoblast projected into the maternal sinusoid. Layer II had abundant glycogen, lipid droplets and lysosomes. Layer III had imbibed much fluid and appeared foamy with swollen organelles. Fibrinoid substance was produced by the giant cells, basophils and the trophoblast bordering the maternal sinusoids. Cyst development was preceded by degeneration of glycogen cells in the basal zone and of the trophoblast in the labyrinthine zone. Pronounced development of gonadotropin/somatotropin granule-like 'secretory granules' and smooth endoplasmic reticulum associated lipid droplets also characterised the labyrinthine trophoblast. The observed placental pathology appears to correlate well with the intrauterine growth retardation and fetal malformations recorded in this animal model.

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链脲佐菌素诱导大鼠妊娠糖尿病胎盘超微结构研究。
Wistar大鼠妊娠第2、4、6 ~ 12天单次注射链脲佐菌素(STZ)诱导糖尿病,第20天收集胎儿和胎盘。对照组要么未经治疗,要么进行载体治疗;或者在STZ注射后,每天给予2-6 IU胰岛素(sc)直到足月。将胎盘固定在戊二醛和多聚甲醛混合物中,电镜下观察超薄切片。经过处理的控制组的结构与未经处理的控制组相似。胰岛素对照组的病理改变与糖尿病组相似,但发生率明显低于糖尿病组。STZ组基底区巨细胞较多;粗内质网内有丰富的扩张池、胞浆内纤维蛋白和核包涵体。滋养海绵细胞内可见大量清晰的空泡、溶酶体和髓磷脂小体。增大的液泡常深深撞击细胞核。糖原细胞解体导致囊肿形成。在迷路区,第1层滋养细胞显示出越来越多的大孔,第2层滋养细胞通过这些大孔投射到母窦。第二层有丰富的糖原、脂滴和溶酶体。第三层吸收了大量的液体,出现泡沫,细胞器肿胀。纤维蛋白样物质由母体窦旁的巨细胞、嗜碱性细胞和滋养细胞产生。囊肿发生前,基底区糖原细胞和迷路区滋养细胞发生变性。促性腺激素/促生长激素颗粒状“分泌颗粒”和光滑的内质网相关脂滴的显著发展也是迷路滋养细胞的特征。观察到的胎盘病理似乎与该动物模型中记录的宫内生长迟缓和胎儿畸形密切相关。
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