Normalization of wall shear stress as a physiological mechanism for regulating maternal uterine artery expansive remodeling during pregnancy.
Normalization of wall shear stress as a physiological mechanism for regulating maternal uterine artery expansive remodeling during pregnancy.
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DOI：
10.1096/fba.2021-00019
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发表时间：
2021-09
影响因子：
2.7
通讯作者：
Osol G
中科院分区：
文献类型：
--
作者：
Khankin EV;Ko NL;Mandalà M;Karumanchi SA;Osol G
妊娠期母体子宫循环的外部重塑对正常的子宫胎盘灌注和妊娠结局至关重要。调节这一过程的生理机制尚不清楚，我们假设它涉及壁切应力（WSS）的正常化。妊娠Sprague-Dawley大鼠在妊娠第10天单侧结扎子宫颈端的主要子宫动脉和静脉，从而将流入/流出子宫角的血液限制在卵巢端的一个点;对侧假手术侧提供内部对照。该手术通过增加WSS改变子宫血流动力学，因为整个子宫角由一条而不是两条血管供应。在妊娠第20天通过活体超声脉冲波多普勒测量动脉直径和血流速度值，并用于计算WSS。虽然卵巢动脉管腔直径和血流速度增加，WSS在两个角相似。这些数据支持的概念，增加WSS继发于血绒膜胎盘是子宫血管重塑的主要生理刺激，其正常化可能是主要的机制，调节动脉周向生长的程度，需要维持胎盘灌注。我们进一步假设，浅螺旋动脉侵入，如先兆子痫，限制了上游剪切应力的增加，导致重塑减弱和胎盘灌注不足。
Outward remodeling of the maternal uterine circulation during pregnancy is essential for normal uteroplacental perfusion and pregnancy outcome. The physiological mechanism by which this process is regulated is unknown; we hypothesized that it involved the normalization of wall shear stress (WSS). Pregnant Sprague–Dawley rats underwent unilateral ligation of the main uterine artery and vein at the cervical end of the uterus on gestational day 10, thus restricting inflow/outflow of blood into that uterine horn to a single point at the ovarian end; the contralateral sham‐operated side provided an internal control. This procedure alters uterine hemodynamics by increasing WSS, since the entire uterine horn is supplied by one rather than two vessels. Arterial diameter and blood flow velocity values were measured by intravital ultrasonographic pulse‐wave Doppler on gestational day 20 and used to calculate WSS. Although both ovarian artery lumen diameter and blood velocity increased, WSS was similar in both horns. These data support the concept that increased WSS secondary to hemochorial placentation is the primary physiological stimulus for uterine vascular remodeling and that its normalization may be the primary mechanism that regulates the extent of arterial circumferential growth required to maintain placental perfusion. We further hypothesize that shallow spiral artery invasion, such as occurs in preeclampsia, limits the increase in upstream shear stress and results in attenuated remodeling and placental under‐perfusion.