Hvizdošová-Kleščová A, Uhlík J, Malina M, Vulterinová H, Novotný T, Vajner L
Charles University in Prague, Second Faculty of Medicine, Department of Histology and Embryology, V Úvalu 84, Prague 5, Motol, CZ 150 06, Czech Republic.
Exp Toxicol Pathol. 2013 Jan;65(1-2):97-103. doi: 10.1016/j.etp.2011.06.006. Epub 2011 Jul 13.
The increased fetoplacental vascular resistance due to chronic hypoxia cannot be explained by simple hypoxic vasoconstriction, as it sustains to some degree after recovery in normobaric environment. To verify a hypothesis that fetoplacental arteries undergo remodeling of their walls similar to remodeling of pulmonary arteries in hypoxic pulmonary hypertension, we used a model of the chronically hypoxic rat placenta. Han Wistar pregnant rats were exposed to 14-day hypoxia (10% of oxygen) during the 6th to 19th day of pregnancy. Chronic hypoxia elicited in both intraplacental (prelabyrinthine) and chorionic plate (insertion) arteries significant narrowing of their lumina. Irregular thickening of their adventitia due to an increase in collagen fibers as well as ground substance was observed; reticular fibers were fragmented. Because of remodeling of fetoplacental arteries, a model of chronically hypoxic rat placenta could simulate human preplacental hypoxia and consequent effects.
慢性缺氧导致的胎儿-胎盘血管阻力增加不能用单纯的缺氧性血管收缩来解释，因为在常压环境恢复后，这种阻力仍会在一定程度上持续存在。为了验证一个假设，即胎儿-胎盘动脉的血管壁会发生类似于缺氧性肺动脉高压中肺动脉重塑的变化，我们使用了慢性缺氧大鼠胎盘模型。在妊娠第6至19天期间，将雌性Wistar大鼠暴露于14天的低氧环境（10%氧气）中。慢性缺氧导致胎盘内（迷路前）动脉和绒毛膜板（插入处）动脉的管腔显著变窄。观察到由于胶原纤维以及基质增加，其外膜出现不规则增厚；网状纤维断裂。由于胎儿-胎盘动脉的重塑，慢性缺氧大鼠胎盘模型可以模拟人类胎盘前缺氧及其后果。
