期刊
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
卷 205, 期 5, 页码 -出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2011.06.008
关键词
cardiovascular risk; fetal programming; lymphocyte biology; mouse pregnancy; preeclampsia
资金
- Natural Sciences and Engineering Research Council and Canada [NGPIN3219-06]
- Canada Research Chairs Program
- Province of Ontario/Queen's Postdoctoral Fellowship [17691]
OBJECTIVE: Our goal was to define mechanisms that protect murine pregnancies deficient in spiral arterial remodeling from hypertension, hypoxia, and intrauterine growth restriction. STUDY DESIGN: Microultrasound analyses were conducted on virgin, gestation day 2, 4, 7, 9, 10, 12, 14, 16, 18, and postpartum BALB/c (wild type) mice and BALB/c-Rag2(-/-)/Il2rg(-/-) mice, an immunodeficient strain lacking spiral arterial remodeling. RESULTS: Rag2(-/-)/Il2rg(-/-) dams had normal spiral arterial flow velocities, greatly elevated uterine artery flow velocities between gestational day 10-16 and smaller areas of placental flow from gestational day 14 to term than controls. Maternal heart weight and output increased transiently. Conceptus alterations included higher flow velocities in the umbilical-placental circulation that became normal before term and bradycardia persistent to term. CONCLUSION: Transient changes in maternal heart weight and function accompanied by fetal circulatory changes successfully compensate for deficient spiral arterial modification in mice. Similar compensations may contribute to the elevated risk for cardiovascular diseases seen in women and their children who experience preeclamptic pregnancies.
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