Identification of the primary outcomes that result from deficient spiral arterial modification in pregnant mice

被引:32
作者
Croy, B. Anne [1 ]
Burke, Suzanne D. [1 ]
Barrette, Valerie F. [1 ]
Zhang, Jianhong [1 ]
Hatta, Kota [2 ]
Smith, Graeme N. [3 ]
Bianco, Juares [1 ,5 ]
Yamada, Aureo T. [5 ]
Adams, Michael A. [4 ]
机构
[1] Queens Univ, Dept Anat & Cell Biol, Kingston, ON K7L 3N6, Canada
[2] Queens Univ, Dept Microbiol & Immunol, Kingston, ON K7L 3N6, Canada
[3] Queens Univ, Dept Obstet & Gynecol, Kingston, ON K7L 3N6, Canada
[4] Queens Univ, Dept Pharmacol & Toxicol, Kingston, ON K7L 3N6, Canada
[5] Univ Estadual Campinas, Inst Biol, Lab Histochem & Cytochem, Campinas, SP, Brazil
基金
加拿大自然科学与工程研究理事会;
关键词
Fecundity; Immune system; Mean arterial pressure; Placental growth; Vascular remodeling; NATURAL-KILLER-CELLS; TROPHOBLAST INVASION; PLACENTAL GROWTH; INTERFERON-GAMMA; T-CELL; PREECLAMPSIA; RISK; EXPRESSION; DISEASE;
D O I
10.1016/j.preghy.2010.10.002
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Pre-eclampsia, an acute complication of human pregnancy, is associated with incomplete physiological modification of decidual spiral arteries. This is thought to promote oxidative stress from perfusion/reperfusion of the placenta and to restrict placental and fetal growth. Alymphoid (genotype Rag2 (/) /Il2rg (/)) mice, sufficient in dendritic and myeloid cell functions, lack spiral arterial modification with individual spiral arteries having similar to 1.7 x the vascular resistance and 0.66 x the blood velocity of +/+ mice. Their placentae are not measurably hypoxic and neither placental growth nor fetal survival is impaired and gestational hypertension is not seen. Thus, lymphocytes rather than vascular adaptations appear to be the pivotal contributors to the clinical complications of pre-eclampsia. (C) 2010 International Society for the Study of Hypertension in Pregnancy. Published by Elsevier B.V. All rights reserved
引用
收藏
页码:87 / 94
页数:8
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