High-end arteriolar resistance limits uterine artery blood flow and restricts fetal growth in preeclampsia and gestational hypertension at high altitude

High-end arteriolar resistance limits uterine artery blood flow and restricts fetal growth in preeclampsia and gestational hypertension at high altitude
复制标题

DOI:
10.1152/ajpregu.91046.2008
复制
发表时间:
2011-05-01
影响因子:
2.8
通讯作者:
Moore, Lorna G.
Moore, Lorna G.
中科院分区:
医学3区
文献类型:
--
作者:
Browne, Vaughn A.;Toledo-Jaldin, Lilian;Moore, Lorna G.

文献摘要

被引文献

相似文献

Browne VA,Toledo-Jaldin L,Davila RD,洛佩斯LP,Yamashiro H,Cioffi-Ragan D,Julian CG,Wilson MJ,Bigham AW,Shriver MD,Honigman B,Vargas E,Roach R,摩尔LG。高海拔地区先兆子痫和妊娠期高血压中,高端小动脉阻力限制子宫动脉血流并限制胎儿生长。Am J Physiol Regul Integr Comp Physiol 300:R1221-R1229,2011年。首次发表于2011年2月16日; doi:10.1152/ajpregu.91046.2008。在高海拔地区,婴儿出生体重的降低和先兆子痫(PE)的频率增加归因于胎盘缺氧程度更高,子宫动脉(UA)直径更小,UA血流量(QUA)更低。这项横断面病例对照研究测定了居住在海拔3,600 - 4,100 m的安第斯山脉人的UA、髂总动脉(CI)和髂外动脉(EI)动脉血流,这些人要么未怀孕(NP,n = 23),要么经历了血压正常的妊娠(NORM; n = 155)、先兆子痫(PE,n = 20)或妊娠期高血压(GH,n = 12)。妊娠使UA直径增大至0.62 cm,但PE或GH的动脉末端血管阻力指数高于NORM。早发性(34周)疾病的Q(UA)较低。正常组左侧Q(UA)始终大于右侧,但PE组的模式相反。尽管PE和GH的Q(CI)和Q(EI)高于NORM,但分配给UA的Q(CI)分数减少了2- 3倍。早发性PE的妇女早产,43%的死胎小于胎龄儿(SGA)。妊娠期生长激素和晚发性肺栓塞患者足月分娩,但SGA发生率较高(GH = 50%,肺栓塞= 46% vs. NORM = 15%,均P < 0.01)。出生体重与Q(UA)降低密切相关(R(2)= 0.80,P < 0.01),疾病严重程度和不良胎儿结局也是如此。我们认为PE和GH的高动脉末端阻力,而不是较小的UA直径,限制Q(UA)和限制胎儿生长。据我们所知,这是第一次定量测量Q(UA)和盆腔血流量的早发性与晚发性PE在高海拔地区的居民。
Browne VA, Toledo-Jaldin L, Davila RD, Lopez LP, Yamashiro H, Cioffi-Ragan D, Julian CG, Wilson MJ, Bigham AW, Shriver MD, Honigman B, Vargas E, Roach R, Moore LG. High-end arteriolar resistance limits uterine artery blood flow and restricts fetal growth in preeclampsia and gestational hypertension at high altitude. Am J Physiol Regul Integr Comp Physiol 300: R1221-R1229, 2011. First published February 16, 2011; doi:10.1152/ajpregu.91046.2008.-The reduction in infant birth weight and increased frequency of preeclampsia (PE) in high-altitude residents have been attributed to greater placental hypoxia, smaller uterine artery (UA) diameter, and lower UA blood flow (QUA). This cross-sectional case-control study determined UA, common iliac (CI), and external iliac (EI) arterial blood flow in Andeans residing at 3,600-4,100 m, who were either nonpregnant (NP, n = 23), or experiencing normotensive pregnancies (NORM; n = 155), preeclampsia (PE, n = 20), or gestational hypertension (GH, n = 12). Pregnancy enlarged UA diameter to similar to 0.62 cm in all groups, but indices of end-arteriolar vascular resistance were higher in PE or GH than in NORM. Q(UA) was lower in early-onset ( 34 wk) illness. Left Q(UA) was consistently greater than right in NORM, but the pattern reversed in PE. Although Q(CI) and Q(EI) were higher in PE and GH than NORM, the fraction of Q(CI) distributed to the UA was reduced 2- to 3-fold. Women with early-onset PE delivered preterm, and 43% had stillborn small for gestational age (SGA) babies. Those with GH and late-onset PE delivered at term but had higher frequencies of SGA babies (GH = 50%, PE = 46% vs. NORM = 15%, both P < 0.01). Birth weight was strongly associated with reduced Q(UA) (R(2) = 0.80, P < 0.01), as were disease severity and adverse fetal outcomes. We concluded that high end-arteriolar resistance, not smaller UA diameter, limited Q(UA) and restricted fetal growth in PE and GH. These are, to our knowledge, the first quantitative measurements of Q(UA) and pelvic blood flow in early-vs. late-onset PE in high-altitude residents.