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

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 ∼1.7× the vascular resistance and 0.66× 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.