POST-IMPLANTATION MODIFICATION OF THE SPIRAL ARTERIES

灵长类动物胎盘的血液供应是由 肌肉螺旋动脉转变为扩张的漏斗- 形状的子宫胎盘动脉，其管壁主要由 滋养层细胞和结缔组织。这些变化是 被认为可以适应更大的血流量 发展的概念所要求的，并修改规范 这些血管的母体控制机制。一直以来 观察到仅有先兆子痫合并妊娠，或 先兆子痫合并高血压，结构调整 动脉壁的范围较小，这显然 影响子宫胎盘的血流灌注。中的关键元素 动脉的转换是血管内细胞的迁移， 被认为是滋养细胞，进入螺旋动脉。这个 内皮细胞明显被移除，紧随其后的是 肌性动脉壁的破坏，并用 滋养层和结缔组织。我们的计划有很多空白 对子宫胎盘动脉发育的认识 在灵长类动物中，尤其是通过细胞机制 进行入侵、破坏和更替。长的- 本提案的术语目标是描述 恒河猴螺旋动脉的侵袭和修饰 猴，一种在胎盘解剖上与 人类。具体目标是1)从超结构上定义 免疫细胞化学：细胞相互作用的顺序 血管内滋养细胞与血管内皮细胞之间的关系 螺旋动脉的初始侵袭；2)确定细胞 血管内滋养层细胞清除血管内滋养细胞 母体内皮细胞，穿透动脉壁和 破坏中膜的平滑肌肉。目前 时间，几乎没有关于这是如何发生的信息 在灵长类动物身上完成的。仔细的超微结构描述 将结合细胞化学研究来评估其作用 溶酶体酶在这一过程中的作用，研究表明 其他物种；3)用免疫细胞化学方法确定 方法：观察结缔组织成分的变化 螺旋动脉转换过程中动脉壁的成分 子宫胎盘动脉的动脉。

The blood supply to the primate placenta is established by the conversion of the muscular spiral arteries into dilated funnel- shaped uteroplacental arteries whose walls are composed mainly of trophoblast cells and connective tissue. These changes are thought to accommodate the greater volume of blood flow required by the developing conceptus, and to modify the normal maternal control mechanisms of these vessels. It has been observed that pregnancies complicated by preeclampsia alone, or preeclampsia with essential hypertension, structural modification of the arterial walls is less extensive and this apparently compromises uteroplacental perfusion. The key element in the conversion of the arteries is the migration of endovascular cells, thought to be trophoblast, into the spiral arteries. The endothelium is apparently removed and this is followed by the destruction of the muscular arterial wall and its replacement by trophoblast and connective tissue. There are many gaps in our understanding of the development of the uteroplacental arteries in primates especially the cellular mechanisms by which the invasion, destruction and replacement are carried out. The long- term objective of this proposal is the characterize the process of invasion and modification of the spiral arteries in the rhesus monkey, a species with many placental anatomical similarities to the human. Specific aims are 1) to define ultrastructurally and immunocytochemically the sequence of cellular interactions between endovascular trophoblast and endothelial cells during the initial invasion of the spiral arteries; 2) to determine the cellular mechanisms by which the endovascular trophoblast removes the maternal endothelium, penetrates the walls of the arteries and destroys the smooth muscle of the tunica media. At the present time, there is little information available on how this is accomplished in primates. Careful ultrastructural descriptions will be coupled with cytochemical studies to evaluate the role of lysosomal enzymes in this process, a role suggested by studies in other species; and 3) to determine, using immunocytochemical methods, the changes in the composition of the connective tissue components of the arterial wall during the conversion of the spiral arteries to the uteroplacental arteries.