Sprague Benjamin J, Phernetton Terrance M, Magness Ronald R, Chesler Naomi C
Department of Biomedical Engineering, University of Wisconsin, Madison, WI, USA.
Eur J Obstet Gynecol Reprod Biol. 2009 May;144 Suppl 1(Suppl 1):S170-8. doi: 10.1016/j.ejogrb.2009.02.041. Epub 2009 Mar 17.
Uterine vascular resistance (UVR) is the ratio of systemic mean arterial pressure to mean uterine blood flow and is sensitive to changes in small arteries and arterioles. However, it provides little or no insight into changes in large, conduit arteries. Fluctuations in estrogen (E2) and progesterone (P4) levels during the ovarian cycle are thought to cause uterine resistance artery vasodilation; the effects on large arteries are unknown. Herein, our objective was to use the uterine vascular impedance, which is sensitive to changes in small and large arteries, to determine the effects of the ovarian cycle and pregnancy on the entire uterine vasculature.
Uterine vascular perfusion pressure and flow rate were recorded simultaneously in anesthetized sheep in the nonpregnant (NP) luteal (NP-L, n=6) and follicular (NP-F, n=7) phases and in late pregnancy (CP, n=10). Impedance and metrics of impedance (input impedance Z(0), index of wave reflection R(W), characteristic impedance Z(C)) were calculated. E2 and P4 levels were measured from jugular vein blood samples. Finally, from pressure-diameter tests post-mortem, large uterine artery circumferential elastic modulus (E(Circ)) was measured. Significant differences were evaluated by two-way ANOVA or Student's t-test.
As expected, E2:P4 was higher in the NP-F group compared to the NP-L group (p<0.05). Also as expected, UVR and Z(0) decreased in the follicular phase compared to the luteal (p<0.05), but R(W), Z(C), and E(Circ) were unaltered. Pregnancy not only substantially decreased UVR (and Z(0)) (p<0.00001) but also decreased Z(C) (p<0.001), R(W) (p<0.0001), E(Circ) (p<0.01), and pulse wave velocity (p<0.0001).
The E2:P4 ratio mediates resistance artery vasodilatation in nonpregnant states, but has no effect on conduit artery size or stiffness. In contrast, pregnancy causes dramatic vasodilation and remodeling, including substantial reductions in conduit artery stiffness and increases in conduit artery size, which affect pulsatile uterine hemodynamics.
子宫血管阻力(UVR)是体循环平均动脉压与子宫平均血流之比,对小动脉和微动脉的变化敏感。然而,它对大的输送动脉的变化几乎没有或根本没有提供见解。卵巢周期中雌激素(E2)和孕激素(P4)水平的波动被认为会导致子宫阻力动脉血管舒张;对大动脉的影响尚不清楚。在此,我们的目的是使用对小动脉和大动脉变化敏感的子宫血管阻抗,来确定卵巢周期和妊娠对整个子宫血管系统的影响。
在麻醉的绵羊中,同时记录非妊娠(NP)黄体期(NP-L,n = 6)和卵泡期(NP-F,n = 7)以及妊娠晚期(CP,n = 10)的子宫血管灌注压和流速。计算阻抗和阻抗指标(输入阻抗Z(0)、波反射指数R(W)、特性阻抗Z(C))。从颈静脉血样中测量E2和P4水平。最后,通过死后压力-直径测试,测量子宫大动脉圆周弹性模量(E(Circ))。通过双向方差分析或学生t检验评估显著差异。
正如预期的那样,NP-F组的E2:P4高于NP-L组(p<0.05)。同样如预期的那样,与黄体期相比,卵泡期的UVR和Z(0)降低(p<0.05),但R(W)、Z(C)和E(Circ)未改变。妊娠不仅显著降低了UVR(和Z(0))(p<0.00001),还降低了Z(C)(p<0.001)、R(W)(p<0.0001)、E(Circ)(p<0.01)和脉搏波速度(p<0.0001)。
E2:P4比值在非妊娠状态下介导阻力动脉血管舒张,但对输送动脉的大小或硬度没有影响。相比之下,妊娠会导致显著的血管舒张和重塑,包括输送动脉硬度的大幅降低和输送动脉大小的增加,这会影响子宫搏动性血流动力学。