Ultrastructure of uteroplacental arteries.
Ultrastructure of uteroplacental arteries.
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子宫胎盘动脉的超微结构。
DOI：
10.1159/000406847
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
W. B. Robertson
中科院分区：
文献类型：
--
作者：
F. de Wolf;I. Brosens;W. B. Robertson
胎盘床螺旋动脉的超微结构研究证实，非绒毛细胞滋养细胞参与了正常妊娠期间这些血管发生的生理变化的发展。在血管内滋养细胞到达之前，但在迁移的间质滋养细胞侵入肌层之后，在螺旋动脉肌层段观察到的变化，其特征是管腔变宽、内膜水肿、弹性膜破坏和介质细胞间隙变宽。这种血管扩张可以促进血管内滋养细胞随后的逆行迁移。胎儿细胞在血管腔内迁移并渗入内皮下间隙，进一步破坏动脉内膜和中膜。改变后的内膜随后由内皮细胞恢复。通过这种方式，细胞滋养细胞被纳入胎盘床螺旋动脉的壁，螺旋动脉由小的肌肉动脉转变为膨胀的透明化管。在妊娠合并先兆子痫和一些妊娠合并胎儿生长迟缓，这些生理变化很大程度上局限于蜕膜节段，而子宫肌段不受影响。急性动脉粥样硬化病变的特征是内膜增厚和中膜坏死。内膜增厚是由于纤维蛋白和其他血浆成分沉积并迁移到巨噬细胞和肌内膜细胞的内膜，这些细胞在细胞质中积累脂肪成为泡沫细胞。临床和实验研究表明，这些病变可由几种引起内皮损伤的因素引起。
Ultrastructural study of the placental bed spiral arteries confirms that non-villous cytotrophoblast is involved in the development of the physiological changes occurring in these vessels during normal pregnancy. The changes observed in the myometrial segments of the spiral arteries before the time of arrival of endovascular trophoblast but after the invasion of the myometrium by migrating interstitial trophoblast, are characterised by widening of the lumen, oedema of the intima, disruption of the elastica and widening of the intercellular spaces of the media. This vascular distension could facilitate the subsequent retrograde migration of endovascular trophoblast. The fetal cells migrate in the vessel lumen and infiltrate the subendothelial space causing further disruption of the arterial intima and media. The altered intima is subsequently recovered by the endothelium. In this way, the cytotrophoblast is incorporated into the wall of the placental bed spiral arteries which are converted from small muscular arteries into distended hyalinized tubes. In pregnancies complicated by preeclampsia and in some pregnancies complicated by fetal growth retardation, these physiological changes are largely restricted to the decidual segments leaving the myometrial segments unaffected. The lesion of acute atherosis is characterised by thickening of the intima and necrosis of the media. The intimal thickening is due to deposition of fibrin and other plasma constituents and migration into the intima of macrophages and myointimal cells which accumulate fat in their cytoplasm to become foam cells. Clinical and experimental studies indicate that these lesions can be initiated by several factors which cause endothelial injury.