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子宫胎盘动脉的超微结构

Ultrastructure of uteroplacental arteries.

作者信息

De Wolf F, Brosens I, Robertson W B

出版信息

Contrib Gynecol Obstet. 1982;9:86-99.

PMID:6754251
Abstract

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.

摘要

胎盘床螺旋动脉的超微结构研究证实,非绒毛细胞滋养层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过程。在血管内滋养层细胞到达之前,但在迁移的间质滋养层细胞侵入子宫肌层之后,在螺旋动脉的子宫肌层段观察到的变化特征为管腔增宽、内膜水肿、弹性组织破坏以及中膜细胞间隙增宽。这种血管扩张可能有助于随后血管内滋养层细胞的逆行迁移。胎儿细胞在血管腔内迁移并浸润内皮下间隙,导致动脉内膜和中膜进一步破坏。随后,改变的内膜由内皮细胞修复。通过这种方式,细胞滋养层细胞被纳入胎盘床螺旋动脉壁,这些动脉从小肌性动脉转变为扩张的玻璃样化管道。在子痫前期合并妊娠以及一些胎儿生长受限合并妊娠中,这些生理变化很大程度上局限于蜕膜段,子宫肌层段未受影响。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的沉积以及巨噬细胞和平滑肌内膜细胞迁移到内膜,这些细胞在其细胞质中积累脂肪而成为泡沫细胞。临床和实验研究表明,这些病变可由多种导致内皮损伤的因素引发。

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Ultrastructure of uteroplacental arteries.子宫胎盘动脉的超微结构
Contrib Gynecol Obstet. 1982;9:86-99.
2
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Endovascular trophoblast invasion: implications for the pathogenesis of intrauterine growth retardation and preeclampsia.血管内滋养层细胞浸润:对胎儿宫内生长受限和子痫前期发病机制的影响。
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An ultrastructural study of utero-placental spiral arteries in hypertensive and normotensive pregnancy and fetal growth retardation.高血压妊娠、正常血压妊娠及胎儿生长受限中子宫胎盘螺旋动脉的超微结构研究
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Divergent trophoblast invasion and apoptosis in placental bed spiral arteries from pregnancies complicated by maternal anemia and early-onset preeclampsia/intrauterine growth restriction.孕期合并母体贫血及早发型子痫前期/胎儿生长受限的胎盘床螺旋动脉中滋养层细胞的侵袭和凋亡存在差异。
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Fibrinolysis in decidual spiral arteries in late pregnancy.妊娠晚期蜕膜螺旋动脉中的纤维蛋白溶解作用。
Thromb Haemost. 1978 Jun 30;39(3):751-8.

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2
Imbalances in circulating angiogenic factors in the pathophysiology of preeclampsia and related disorders.循环血管生成因子失衡与子痫前期及相关疾病的病理生理学。
Am J Obstet Gynecol. 2022 Feb;226(2S):S1019-S1034. doi: 10.1016/j.ajog.2020.10.022. Epub 2020 Oct 20.
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J Reprod Immunol. 2010 May;85(1):112-6. doi: 10.1016/j.jri.2010.01.002. Epub 2010 Mar 16.
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Am J Hypertens. 2007 Nov;20(11):1216-21. doi: 10.1016/j.amjhyper.2007.07.002.
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Curr Hypertens Rep. 2006 May;8(2):144-52. doi: 10.1007/s11906-006-0011-1.