Ultrastructure of uteroplacental arteries.
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.
D001158:Arteries / Q000378:metabolism / Q000648:ultrastructure*; D001161:Arteriosclerosis / Q000209:etiology / Q000473:pathology; D004727:Endothelium / Q000648:ultrastructure; D005260:Female; D005317:Fetal Growth Retardation / Q000473:pathology; D005337:Fibrin / Q000378:metabolism; D006801:Humans; D008854:Microscopy, Electron; D010920:Placenta / Q000098:blood supply*; D011225:Pre-Eclampsia / Q000473:pathology; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000473:pathology; D014327:Trophoblasts / Q000098:blood supply / Q000502:physiology; D014599:Uterus / Q000098:blood supply*
D005337:Fibrin