Kharfi Abdelaziz, Giguère Yves, Sapin Vincent, Massé Jacques, Dastugue Bernard, Forest Jean-Claude
Unité de périnatalogie, Centre de Recherche de l'Hôpital Saint-François d'Assise, CHUQ, Québec, Canada.
Clin Biochem. 2003 Jul;36(5):323-31. doi: 10.1016/s0009-9120(03)00060-2.
To summarize the recent knowledge on the implications of placenta and cytokines in normal and preeclamptic pregnancies.
A literature search was conducted of applicable articles related to interactions between trophoblast and cytokines in generating preeclampsia.
The initiating event in preeclampsia has been postulated to be the reduced uteroplacental perfusion as a result of abnormal extravillous cytotrophoblast invasion and remodeling of the uterine spiral arteries. Focal ischemia and hypoxia, deportation of hypoxemic trophoblast cells and abnormal expression of various placental biologic molecules, particularly the cytokines, are thought to lead to widespread dysfunction of the maternal vascular endothelium resulting in overproduction of endothelin and thromboxane, enhanced vascular sensitivity to angiotensin II, and reduced secretion of vasodilators such as nitric oxide and prostacyclin. These alterations, in turn, cause hypertension, proteinuria and edema, and pathologies in many organ systems (kidney, lung, liver, brain).
总结近期关于胎盘和细胞因子在正常妊娠和子痫前期妊娠中的影响的知识。
对与滋养层细胞和细胞因子在子痫前期发生过程中的相互作用相关的适用文章进行了文献检索。
子痫前期的起始事件被推测为由于绒毛外细胞滋养层侵袭异常和子宫螺旋动脉重塑导致子宫胎盘灌注减少。局灶性缺血和缺氧、低氧滋养层细胞的排出以及各种胎盘生物分子，特别是细胞因子的异常表达，被认为会导致母体血管内皮广泛功能障碍，从而导致内皮素和血栓素过度产生、血管对血管紧张素II的敏感性增强以及一氧化氮和前列环素等血管舒张剂分泌减少。这些改变进而导致高血压、蛋白尿和水肿，以及许多器官系统（肾脏、肺、肝脏、脑）出现病变。
