Structure adaptation and blood flow control in the uterine arterial system after hemochorial placentation.
In the course of hemochorial placentation, trophoblast cells build a most conductive placental stream bed for maternal blood with intramural foetal capillaries. The stream bed is adapted to the maternal vascular system, causing local increase in flow and shear stress. Subsequently, local maternal microvascular system vanishes. The remaining upstream arteries, up to the aorta, undergo "physiological changes", i.e. increase in circumference and length, predominantly by growth and remodeling. Peripheral uterine arteries, possibly collapsed due to low intraluminal pressure, show over-dilatation associated with endothelium destruction and trophoblast cell invasion. Overall arterial conductance increases to controlled extent; placental blood flow rate rises moderately. Intraplacental blood pressures are kept low allowing for free perfusion of placental foetal capillaries. According to the generally accepted concept, destructing impact of invading trophoblast cells causes the physiological changes. However, trophoblast invasion does not explain physiological changes occurring before and outside trophoblast invasion. On the other hand, physiological changes may well be induced by shear stress, which operates in extrauterine body regions as signal for vascular adaptation to growth. Thus, it is hypothesized that trophoblast cells control vascular adaptation and placental blood flow rate simply by constructing the hemochorial steam bed, thereby building up shear stress and triggering the general physiological automatism for controlled vascular adaptation to growth.
Moll
Waldemar
W
Institut für Physiologie der Universität Regensburg, Universitätsstrasse 31, D-93040 Regensburg, Germany. waldemar.moll@vkl.uni-regensburg.de
D000818:Animals; D001158:Arteries / Q000033:anatomy & histology* / Q000502:physiology*; D005260:Female; D018056:Hemorheology; D006706:Homeostasis; D006801:Humans; D008431:Maternal-Fetal Exchange / Q000502:physiology; D010920:Placenta / Q000098:blood supply; D010929:Placentation / Q000502:physiology*; D011247:Pregnancy; D014327:Trophoblasts / Q000502:physiology; D014599:Uterus / Q000098:blood supply*; D014655:Vascular Resistance