Alterations in maternal and fetal heart functions accompany failed spiral arterial remodeling in pregnant mice.

Abstract

Our goal was to define mechanisms that protect murine pregnancies deficient in spiral arterial remodeling from hypertension, hypoxia, and intrauterine growth restriction. 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. 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. 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.